Beating Melanoma – need to post photos

Thanks for your reply. I hope there will soon be a way to post photos here. In the mean time, I will post what I wrote when I registered. Anybody who are interested in my pictures to tract my progress are welcome to contact me directly at [email protected]  As always I am posting my experience and my personal case and in no way suggesting anyone to follow suit. Our air remains the same though, that being able to get rid of the melanoma and I think I have found the way. 

Below is what I wrote when I registered:

Thanks for your reply. I hope there will soon be a way to post photos here. In the mean time, I will post what I wrote when I registered. Anybody who are interested in my pictures to tract my progress are welcome to contact me directly at [email protected]  As always I am posting my experience and my personal case and in no way suggesting anyone to follow suit. Our air remains the same though, that being able to get rid of the melanoma and I think I have found the way. 

Below is what I wrote when I registered:

Thanks for your reply. I hope there will soon be a way to post photos here. In the mean time, I will post what I wrote when I registered. Anybody who are interested in my pictures to tract my progress are welcome to contact me directly at [email protected]  As always I am posting my experience and my personal case and in no way suggesting anyone to follow suit. Our air remains the same though, that being able to get rid of the melanoma and I think I have found the way. 

Below is what I wrote when I registered:

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

How can I be offended when people are honest with their opinion and experiences!? Most of all you are acting to my benefit and I thank you. I am well aware of how bad melanoma is and can be and that is why I quickly started my treatment even without having a histological report. As to sodium bicarbnoate and iodine being able to get rid of melanoma, some are skeptics and some are converts. I happen to be a convert. I have posted a new photo taken this morning and the lesion has definitely receeded and the color lightened. https://www.shutterfly.com/ photo #16. Will be seeing my dermatologist soon.

Thanks all.  Dennis

How can I be offended when people are honest with their opinion and experiences!? Most of all you are acting to my benefit and I thank you. I am well aware of how bad melanoma is and can be and that is why I quickly started my treatment even without having a histological report. As to sodium bicarbnoate and iodine being able to get rid of melanoma, some are skeptics and some are converts. I happen to be a convert. I have posted a new photo taken this morning and the lesion has definitely receeded and the color lightened. https://www.shutterfly.com/ photo #16. Will be seeing my dermatologist soon.

Thanks all.  Dennis

How can I be offended when people are honest with their opinion and experiences!? Most of all you are acting to my benefit and I thank you. I am well aware of how bad melanoma is and can be and that is why I quickly started my treatment even without having a histological report. As to sodium bicarbnoate and iodine being able to get rid of melanoma, some are skeptics and some are converts. I happen to be a convert. I have posted a new photo taken this morning and the lesion has definitely receeded and the color lightened. https://www.shutterfly.com/ photo #16. Will be seeing my dermatologist soon.

Thanks all.  Dennis

Hi Joan C: No I have not had my melanoma removed yet and my treatment is on the melanoma.  I have posted my photos here: http://melanomabegone.shutterfly.com/   Let me know what you think.  Dennis

Thanks Janner for the reply and concern. No I have not had a biopsy and my disgnosis would be called a "clinical diagnosis" usually to be confirmed or otherwise via a biopsy. With melanoma they usually do an excision biopsy where possible and to do it properly they include a 1 cm border in case it IS melanoma. I am trying to post some pictures as I have been keeping tract of the treatment. Thanks again. Dennis

Thanks Janner for the reply and concern. No I have not had a biopsy and my disgnosis would be called a "clinical diagnosis" usually to be confirmed or otherwise via a biopsy. With melanoma they usually do an excision biopsy where possible and to do it properly they include a 1 cm border in case it IS melanoma. I am trying to post some pictures as I have been keeping tract of the treatment. Thanks again. Dennis

Thanks Janner for the reply and concern. No I have not had a biopsy and my disgnosis would be called a "clinical diagnosis" usually to be confirmed or otherwise via a biopsy. With melanoma they usually do an excision biopsy where possible and to do it properly they include a 1 cm border in case it IS melanoma. I am trying to post some pictures as I have been keeping tract of the treatment. Thanks again. Dennis

I am moved that you are all concern about my well being and me treatment myself as opposed to quickly surgically removing it. I understand that in your opinion quickly surgically excising it is the best option and I respect that. I am taken by your caring and your support for each other. I joined and posted hoping to let you all know that there is another way, not necessarily as an alternative but as an additional to the traditional.

One replied "I have just read thru the links you posted.  I find that quack-science.  You need more than iodine to cure cancer.  It is insulting to people fighting the cancer fight to declare that "cancer is curable" in a blanket statement like that, and if they are not using your bogus methods then they will lose their fight." 

I would like to address this reply and kind of thinking. What I have presented is not "quack-science" just because "main stream medicine" and yourself do not believe in it's cancer curing ability.  The last thing I want is to be "insulting to people fighting the cancer fight".  However cancer IS curable. (See below.) There are numerous ways to fight cancer and nowhere in my previous post did I ever said that "if they are not using your [my] bogus methods then they will lose their fight" When it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire. I am sorry I made you so angry.

My treatment is based on what is advocated by Dr. Simoncini and Dr. Sircus with additions using what other resources I have at my disposal. It works because sodium bicarbonate is a natural substance produced by the body, the maple syrup (sugar) is for the cancer cells as a Trojan Horse to get the sodium bicarbonate into the cancer cells and the iodine is a topical attack from the surface in. Without sodium bicarbonate you will die. It is used in emergency rooms, resuscitations, cases of acidosis, as well as with chemo therapy so they do not poison the whole patient. Not enough bicarbonate leads to diseases and illnesses ultimately to cancer. Remember that the mind, like a parachute functions only when opened.

You can read them here:

Dr. Simoncini:  http://www.curenaturalicancro.com/index.php

http://www.youtube.com/watch?v=npgyZMaewuE&feature  

Sodium bicarbonate, a natural way to treat the cancer

http://www.imva.info/news/sodium-bicarbonate-baking-soda-cancer-treatment.html

and

http://publications.imva.info/index.php/e-books/sodium-bicarbonate-rich-man-s-poor-man-s-cancer-treatment-e-book.html

I joined this blog to learn from you all with an open mind as well as I hope to contribute back by posting additional modalities of treatment SUCH THAT THE CANCER DOES NOT COME BACK. One just posted that after years of having his/her melanoma removed that a new one came up RIGHT WHERE THE ORIGINAL WAS. What a shame that this has to happen. 

I will first supply some of the information I have on melanoma (in no particular order) and end with how (skin) cancer can be beaten. I apologize that it is going to be long and I hope that for those with an open mind  and want to know as much as possible so you can make a truly informed decision that they find at least some of the following research beneficial. Most are on melanoma while others are to show that cancer CAN indeed be beaten so as not to give up hope. Still others are on what influences the development or prevention of cancer that you yourself can take a proactive role for your own health. For those who do not have the time you may wish to just scan the web sites above of Dr. Simoncini and Dr. Sircus or scroll to the bottom to see the effective treatment of Dr. Simoncini put into practice (and YES) curing skin cancer. Cancer CAN be beaten. It happens everyday.

http://informahealthcare.com/doi/abs/10.1080/13590840802305423

Pharmacokinetics of oral vitamin C

Journal of Nutritional and Environmental Medicine

2008, Vol. 17, No. 3 , Pages 169-177

To determine whether plasma levels above 280 µm L⁻¹, which have selectively killed cancer, bacteria or viruses (in laboratory experiments), can be achieved using oral doses of vitamin C.these information beneficial, which is my purpose in joining this blog, to contribute and to learn in return.

http://oncologystat.com/news/Multiple_Melanomas_in_the_Same_Patient_a_Real_Phenomenon_US.html  Multiple Melanomas in the Same Patient a Real Phenomenon

The chances of a patient's developing multiple primary melanomas over a lifetime is a real phenomenon, with an incidence ranging from 2% to 8% among patients who have had a first melanoma, or an average of about 5%.

Of patients who develop additional melanomas, about 80% develop one in addition to the original, 15% develop two, and the remainder develop three or more. "In my practice I have about four people I follow who have had five or six primary melanomas," said Dr. Burrows, who has practiced dermatology for nearly 40 years and is currently with the division of dermatology at Scripps Clinic Rancho Bernardo in San Diego.

http://oncologystat.com/journals/review_articles/YCTRV/Methods_of_detection_of_circulating_melanoma_cells_A_comparative_overview.html

Methods of detection of circulating melanoma cells: A comparative overview

Cancer Treat Rev. 2011 Jun;37(4):284-290, Andrianos Nezos, Pavlos Msaouel, Nikolaos Pissimissis, Peter Lembessis, Antigone Sourla, Athanasios Armakolas, Helen Gogas, Alexandros J. Stratigos, Andreas D. Katsambas, Michael Koutsilieris

Abstract

Disease dissemination is the major cause of melanoma-related death. A crucial step in the metastatic process is the intravascular invasion and circulation of melanoma cells in the bloodstream with subsequent development of distant micrometastases that is initially clinically undetectable and will eventually progress into clinically apparent metastasis. Therefore, the use of molecular methods to detect circulating melanoma cells may be of value in risk stratification and clinical management of such patients. Herein, we review the currently applied techniques for the detection, isolation, enrichment and further characterization of circulating melanoma cells from peripheral blood samples in melanoma patients. Furthermore, we provide a brief overview of the various molecular markers currently being evaluated as prognostic indicators of melanoma progression.

http://oncologystat.com/journals/review_articles/AEP/Vitamin_D_and_Melanoma.html

Vitamin D and Melanoma

Ann Epidemiol. 2009 Jul;19(7):455-461, Kathleen M. Egan

Abstract

Purpose

Ultraviolet light from sunlight and other sources is the major environmental risk factor for melanoma of the skin. Humans also derive most of their vitamin D from exposure to sunlight. This article reviews current evidence that vitamin D might play a preventive role in the development of melanoma or affect tumor aggressiveness or melanoma patient outcomes.

Methods

Literature review.

Results

The vitamin D receptor has been identified in normal melanocytes as well as melanoma cell lines and primary tissue. A few studies have demonstrated relationships of functional polymorphisms in the vitamin D receptor with melanoma risk or tumor aggressiveness. Identifying an independent influence of vitamin D on melanoma risk is hampered by overwhelming confounding by the carcinogenic influence of ultraviolet radiation on skin melanocytes. Nonetheless an inverse association was suggested in a few studies with greater consumption of dairy foods or other dietary sources. Several lines of evidence are consistent with a potential influence for vitamin D on site-specific aggressiveness of skin melanomas, therapeutic response or patient survival.

Conclusion

Additional research is needed to determine whether vitamin D may have a preventive role in melanoma incidence or a salutary influence on melanoma patient outcome.

http://www.youtube.com/watch?v=KOUR9JSmY3w&feature

Connection with Vitamin D and Cancer

http://articles.mercola.com/sites/articles/archive/2011/11/20/deadly-melanoma-not-due-vitamin-d-deficiency.aspx

The Surprising Cause of Melanoma (And No, it's Not Too Much Sun) Posted By Dr. Mercola | November 20 2011 

http://mercola.fileburst.com/PDF/ExpertInterviewTranscripts/InterviewCaroleBaggerlyVitaminD.pdf

A Special Interview with Carole Baggerly  By Dr. Mercola on Vitamin D and Cancer

http://oncologystat.com/journals/review_articles/SOC/Surgical_Approach_to_Primary_Cutaneous_Melanoma.html

Surgical Approach to Primary Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):39-56, Patrick A. Ott, Russell S. Berman

Abstract

The surgical management of primary cutaneous melanoma, from the diagnostic biopsy through the wide local excision and nodal staging, must be carefully planned, and the biology of the melanoma, microstaging and primary tumor pathologic features of the melanoma, location on the body, patient preferences, and comorbidities must be considered. The treating surgeon must balance preservation of oncologic principles, with optimization of functional and aesthetic outcome. This article reviews the rationale behind the surgical approach in the patient with a primary melanoma.

http://oncologystat.com/journals/ew/YSDIA/Falsepositive_cells_in_sentinel_lymph_nodes.html

False-positive cells in sentinel lymph nodes

Semin Diagn Pathol. 2008 May;25(2):116-119, Jeoffry B. Brennick, Shaofeng Yan

Melanoma sentinel lymph nodes (SLN) are carefully evaluated to maximize sensitivity. Examination includes hematoxylin and eosin (H+E) stained sections at multiple levels through the node, with subsequent immunohistochemical (IHC) stains for melanocytic markers if H+E sections are negative for melanoma. However, not all IHC-positive cells in SLN are metastatic melanoma, as evidenced by the presence of MART-1 positive cells in SLN from breast cancer patients with no history of melanoma (so-called ‘false-positive’ cells). These ‘false-positive cells’ could be nodal nevus, non-melanocytic cells with cross-reacting antigenic determinants, phagocytic cells containing melanocyte antigens, or possibly melanocytes or melanocyte stem cells liberated at the time of biopsy of the cutaneous melanoma. Examination of SLN requires careful correlation of H+E and IHC findings.

http://oncologystat.com/journals/review_articles/SOC/Staging_and_Prognosis_of_Cutaneous_Melanoma.html

Staging and Prognosis of Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):1-17, Paxton V. Dickson, Jeffrey E. Gershenwald

Abstract

Staging of cutaneous melanoma continues to evolve through identification and rigorous analysis of potential prognostic factors. In 1998, the American Joint Committee on Cancer (AJCC) Melanoma Staging Committee developed the AJCC melanoma staging database, an international integrated compilation of prospectively accumulated melanoma outcome data from several centers and clinical trial cooperative groups. Analysis of this database resulted in major revisions to the TNM staging system reflected in the sixth edition of the AJCC Cancer Staging Manual published in 2002. More recently, the committee's analysis of an updated melanoma staging database, including prospective data on more than 50,000 patients, led to staging revisions adopted in the seventh edition of the AJCC Cancer Staging Manual published in 2009. This article highlights these revisions, reviews relevant prognostic factors and their impact on staging, and discusses emerging tools that will likely affect future staging systems and clinical practice.

http://oncologystat.com/journals/review_articles/SOC/EvidenceBased_Followup_for_the_Patient_with_Melanoma.html

Evidence-Based Follow-up for the Patient with Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):181-200, Ryan C. Fields, Daniel G. Coit

Abstract

This article reviews the best evidence available to guide the follow-up of patients with melanoma, focusing on incidence of, and detection of, melanoma recurrence, frequency of follow-up visits, yield of, laboratory and radiographic tests, outcomes of patients with recurrent melanoma based on method of detection, detection of secondary melanomas, and stage-specific follow-up.

http://www.surgonc.theclinics.com/article/S1055-3207(10)00091-8/ppt

Immunotherapy of Melanoma: An Update

·       Jade Homsi, MD, Joshua C. Grimm, BA, Patrick Hwu, MD

     The incidence of melanoma has been increasing worldwide. A relationship between melanoma and the immune system was established years ago. Modulating the immune system in the management of different stages of melanoma has been the focus of numerous large randomized trials worldwide. This article reviews the current status of immunotherapy for melanoma, with a focus on the recent promising results from using vaccines, cytotoxic T-lymphocyte antigen-4 (CTLA-4) antibodies, and adoptive cell therapy.

http://www.ncbi.nlm.nih.gov/pubmed/18022553

Surg Oncol Clin N Am. 2007 Oct;16(4):945-73, xi.

Current immunotherapeutic strategies in malignant melanoma.

Agostino NM, Ali A, Nair SG, Mosca PJ.

Source

Department of Internal Medicine, Lehigh Valley Hospital and Health Network, 1240 South Cedar Crest Boulevard, Allentown, PA 18103, USA.

Abstract

The basis of immunotherapy for melanoma is the existence of melanoma-associated antigens that can be targeted by the immune system. Identification of many of these antigens has enabled investigators to develop a wide array of immunotherapy strategies for the treatment of melanoma. Although several of these strategies have been shown to induce antitumor immune responses in some patients, robust clinical responses have been observed less frequently. With exciting recent advancements in this field, however, there is promise of generating potent immunologic responses and translating them more consistently into durable clinical responses. This article reviews several current approaches to immunotherapy for melanoma and describes the key role that surgeons play in advancing this area of oncology.

http://www.oncologystat.com/journals/journal_scans/Ulceration_and_Stage_Are_Predictive_of_Interferon_Efficacy_In_Melanoma_Results_of_the_Phase_III_Adjuvant_Trials_EORTC_18952_and_EORTC_18991.html 

Ulceration and Stage Are Predictive of Interferon Efficacy In Melanoma: Results of the Phase III Adjuvant Trials EORTC 18952 and EORTC 18991

Breast. 2011 Oct 1;20(3), AMM Eggermont, S Suciu, A Testori, A Spatz, et al

TAKE-HOME MESSAGE

This combined analysis of two large prospective trials of adjuvant interferon for treatment of patients with resected melanoma demonstrated that tumor stage and ulceration predict for immunotherapy benefit.

Abstract

Summary: Adjuvant interferon has modest activity in melanoma patients at high risk for relapse. Patient selection is important; stage and ulceration of the primary tumour are key prognostic factors.

Methods: In this post hoc meta-analysis of European Organisation for Research and Treatment of Cancer (EORTC) trials 18952 (intermediate doses of interferon α-2b [IFN] versus observation in stage IIb-III patients) and 18991 (pegylated [PEG]-IFN versus observation in stage III patients), the predictive value of ulceration on the efficacy of IFN/PEG-IFN with regard to relapse-free survival (RFS), distant metastasis-free survival (DMFS), and overall survival (OS) was assessed in the overall population and in subgroups stratified by stage (IIb and III-N1 [microscopic nodal disease] and III-N2 [macroscopic nodal disease]).

Findings: In the overall population, the comparison of IFN/PEG-IFN versus observation for RFS, DMFS and OS yielded estimated hazard ratios (HR) of 0.85 (p=0.004), 0.89 (p=0.04) and 0.94 (p=0.36), respectively. The impact of treatment was greater in the ulceration group (n=849) compared with the non-ulceration group (n=1336) for RFS (test for interaction: p=0.02), DMFS (p<0.001) and OS (p<0.001). The greatest risk reductions were observed in patients with ulceration and stage IIb/III-N1, with estimated HR for RFS, DMFS, and OS of 0.69 (p=0.003), 0.59 (p<0.0001) and 0.58 (p<0.0001), respectively. The efficacy of IFN/PEG-IFN was lower in stage III-N2 patients with ulceration and uniformly absent in patients without ulceration. There was consistency between the data of both trials.

Interpretation: This meta-analysis of the EORTC 18952 and 18991 trials indicated that both tumour stage and ulceration were predictive factors for the efficacy of adjuvant IFN/PEG-IFN therapy.

http://oncologystat.com/journals/review_articles/archive/Metastatic_Melanoma_An_AJCC_Review.html

or  

http://www.communityoncology.net/co/journal/articles/0508441.pdf

Metastatic Melanoma: An AJCC Review

Community Oncology. 2008 Aug 1;5(8):441-445, SS Agarwala

Abstract

Outside clinical trials, current therapeutic options for patients with metastatic melanoma appear to be of limited benefit. Combination chemotherapy has not been shown to improve outcomes over single-agent chemotherapy, and dacarbazine, which is still the only agent approved by the US Food and Drug Administration for this disease, has produced low response rates and little meaningful improvement in survival. However, with the development and testing of several new compounds, both in the area of immunotherapy and targeted therapy, the future for patients with this disease may become brighter.

News Story: Investigational TKI Active Against Advanced Melanoma in Early Trial »

News Story: Tremelimumab Monotherapy Adds No Benefit Over Chemo in Metastatic Melanoma »

Journal Article: Treatment of Metastatic Melanoma With Autologous CD4+ T Cells Against NY-ESO-1 »

Journal Article: Biochemotherapy for the Treatment of Metastatic Malignant Melanoma: A Systematic Review »

Journal Article: Treatments for Metastatic Melanoma: Synthesis of Evidence From Randomized Trials »

Journal Article: Chemotherapy Compared With Biochemotherapy for the Treatment of Metastatic Melanoma: A Meta-analysis of 18 Trials Involving 2,621 Patients »

http://oncologystat.com/journals/review_articles/HOC/Progress_in_Melanoma_Histopathology_and_Diagnosis.html

Progress in Melanoma Histopathology and Diagnosis

Hematol Oncol Clin North Am. 2009 Jun;23(3):467-480, Adriano Piris, Martin C. Mihm

Abstract

The past 15 years have seen rapid advances in both our understanding of hereditary melanoma genetics and the technologies that enable scientists to make discoveries. Despite great efforts by many groups worldwide, other high-risk melanoma loci besides CDKN2A still remain elusive. A panel of polymorphisms that appears to confer low-to-moderate risk for melanoma has been assembled through functional and genome-wide association studies. The goal of personalized melanoma risk prediction is within our reach, although true clinical use has yet to be established.

http://oncologystat.com/news/Melanoma_Field_Cells_May_Explain_Local_Tumor_Recurrence_US.html  Melanoma Field Cells May Explain Local Tumor Recurrence

Elsevier Global Medical News. 2009 Mar 2, B Jancin  MAUI, HAWAII (EGMN) – The recent discovery of an entity called melanoma field cells that are often present in seemingly normal skin surrounding primary melanomas could ultimately force an overhaul of standard recommended excision margins.

These melanoma field cells are morphologically normal junctional melanocytes and thus cannot be identified using histopathologic criteria. Yet they are genetically melanoma as demonstrated using comparative genomic hybridization and fluorescent in situ hybridization, Dr. Maxwell A. Fung explained at the annual Hawaii Dermatology Seminar sponsored by the Skin Disease Education Foundation.

http://ebm.rsmjournals.com/content/234/8/825.full.pdf+html?sid=658bdab7-e25a-4654-bb4c-ac0d3900cbda

Experimental Biology and Medicine

Molecular Targets of Nutraceuticals Derived from Dietary Spices: Potential Role in Suppression of Inflammation and Tumorigenesis

Overall our review suggests “adding spice to your life” may serve as a healthy and delicious way to ward off cancer and other chronic diseases.

http://journals.lww.com/melanomaresearch/Abstract/2007/10000/Curcumin_downregulates_the_constitutive_activity.2.aspx

Melanoma Research:

October 2007 – Volume 17 – Issue 5 – pp 274-283

doi: 10.1097/CMR.0b013e3282ed3d0e

Original Articles

Curcumin downregulates the constitutive activity of NF-[kappa]B and induces apoptosis in novel mouse melanoma cells

Abstract

Melanoma, the most deadly form of skin cancer, is very aggressive and resistant to present therapies. The transcription factor nuclear factor-kappa B (NF-κB) has been reported to be constitutively active in many types of cancer. Constitutively active NF-κB seen in melanoma likely plays a central role in cell survival and growth. We have established and characterized novel cell lines from our murine melanoma model. Here we report the constitutive activity of NF-κB in these melanoma-derived cells, as shown by electrophoretic mobility shift assay and reporter assays. We hypothesized that agents that inhibit NF-κB may also inhibit cell proliferation and may induce apoptosis in such melanoma cells. Curcumin has been shown to inhibit NF-κB activity in several cell types. In our system, curcumin selectively inhibited growth of melanoma cells, but not normal melanocytes. Curcumin induced melanoma cells to undergo apoptosis, as shown by caspase-3 activation, inversion of membrane phosphatidyl serine, and increases in cells in the sub-G₁ phase. A curcumin dose-dependent inhibition of NF-κB-driven reporter activity correlated with decreased levels of phospho-IκBα, and decreased expression of NF-κB-target genes COX-2 and cyclin D1. This study demonstrates that the use of cells from our model system can facilitate studies of signaling pathways in melanoma. We furthermore conclude that curcumin, a natural and safe compound, inhibits NF-κB activity and the expression of its downstream target genes, and also selectively induces apoptosis of melanoma cells but not normal melanocytes. These encouraging in-vitro results support further investigation of curcumin for treatment of melanoma in vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12680238

Anticancer Res. 2003 Jan-Feb;23(1A):363-98.

Anticancer potential of curcumin: preclinical and clinical studies.

Aggarwal BB, Kumar A, Bharti AC.

Cytokine Research Section, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX, USA. [email protected]

Abstract

Curcumin (diferuloylmethane) is a polyphenol derived from the plant Curcuma longa, commonly called turmeric. Extensive research over the last 50 years has indicated this polyphenol can both prevent and treat cancer. The anticancer potential of curcumin stems from its ability to suppress proliferation of a wide variety of tumor cells, down-regulate transcription factors NF-kappa B, AP-1 and Egr-1; down-regulate the expression of COX2, LOX, NOS, MMP-9, uPA, TNF, chemokines, cell surface adhesion molecules and cyclin D1; down-regulate growth factor receptors (such as EGFR and HER2); and inhibit the activity of c-Jun N-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases. In several systems, curcumin has been described as a potent antioxidant and anti-inflammatory agent. Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis. Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day. All of these studies suggest that curcumin has enormous potential in the prevention and therapy of cancer. The current review describes in detail the data supporting these studies.

http://www.experts.scival.com/wayne/pubDetail.asp?t=pm&id=15252141&amp;

Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation.

http://ur.rutgers.edu/medrel/viewArticle.html?ArticleID=49

 Rutgers, The State University of New Jersey: Curry and Cauliflower Could Halt Prostate Cancer

http://www.jcrows.com/curryfightsprostatecancer.html  

Curry fights prostate cancer, study finds

http://mss3.libraries.rutgers.edu/dlr/showfed.php?pid=rutgers-lib:25088  

Prostate cancer chemoprevention by dietary phytochemicals: 

Chemoprevention entails the use of preferably dietary agents to block or suppress the various stages of prostate carcinogenesis. Flavonoids, the essential components of fruits and vegetables can modulate transcription factor AP-1 and its upstream signaling cascades mainly ERK-MAPK and JNK-MAPK in human androgen insensitive prostate cancer (PC3) cells. Soy isoflavone concentrate can upregulate the expression of several phase II detoxifying and antioxidant genes in an NF-E2-related factor 2 (Nrf2) dependent manner. In addition to detoxifying genes, soy isoflavone concentrate can also modulate the expression of genes such as LATS2, GREB1, calpain and many more in an Nrf2 dependent manner. 

In one such transgenic model, curcumin or PEITC suppressed high grade PIN levels. However a combination of low doses of these agents worked remarkably well in suppressing tumors all together.

http://www.newswise.com/articles/view/573327/

Genetic Evidence That Antioxidants Can Help Treat Cancer  

“Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth,” said lead researcher Michael P. Lisanti, M.D., Ph.D., professor of cancer biology at Jefferson Medical College of Thomas Jefferson University and member of the Kimmel Cancer Center at Jefferson. “This means we need to make anti-cancer drugs that specially target this type of oxidative stress. And there are already antioxidant drugs out there on the market as dietary supplements, like N-acetyl cysteine.” 

The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.

“Antioxidants have been associated with cancer reducing effects—beta carotene, for example—but the mechanisms, the genetic evidence, has been lacking,” Dr. Lisanti said. “This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth.”

 These findings were originally published in the online February 15 issue of Cancer Biology & Therapy.

http://cancerres.aacrjournals.org/content/71/13/4484

A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.

http://www.newswise.com/articles/view/574151/?sc=mwhn

Biologists Show How Veggies Work in Cancer-Fighting Diet

Released: 3/7/2011 3:00 PM EST 

Source: University of Alabama at Birmingham

Newswise — BIRMINGHAM, Ala. – Mothers around the world now collectively can say, “I told you so.”

Your vegetables are good for you, says a research review published by scientists from the University of Alabama at Birmingham in the journal Clinical Epigenetics.

In particular, vegetables such as broccoli and cabbage are filled with compounds that could help reverse or prevent cancers and other aging-related diseases as part of the “epigenetics diet,” a new lifestyle concept coined after the article’s publication.

“Your mother always told you to eat your vegetables, and she was right,” says co-author Trygve Tollefsbol, Ph.D., D.O., a biology professor in the UAB College of Arts and Sciences. “But now we better understand why she was right — compounds in many of these foods suppress gene aberrations that over time cause fatal diseases.”

Epigenetics is the study of the changes in human gene expressions with time, changes that can cause cancer and Alzheimer’s, among other diseases. In recent years, epigenetics research worldwide, including numerous studies conducted at UAB, have identified specific food compounds that inhibit negative epigenetic effects.

Those foods include soybeans, cauliflower, broccoli and cabbage. Green tea, fava beans, kale, grapes and the spice turmeric round out the diet.

“The epigenetics diet can be adopted easily, because the concentrations of the compounds needed for a positive effect are readily achievable,” says lead author Syed Meeran, Ph.D., a research assistant professor in Tollefsbol’s UAB Department of Biology laboratory.

For example, Meeran says sipping tea compounds called polyphenols in daily amounts that are equivalent to approximately three cups of green tea has been shown to reverse breast cancer in laboratory mice by suppressing the gene that triggers the disease. Similarly, a daily cup of broccoli sprouts, which has sulforaphane as an active compound, has been shown to reduce the risk of developing many cancers.

“Our review article has drawn everything together from global studies, and the common theme is that compounds in the epigenetics diet foods can, at the very least, help us lead healthier lives and help our bodies prevent potentially debilitating diseases like breast cancer and Alzheimer’s,” Tollefsbol says.

http://www.nature.com/onc/journal/v24/n48/abs/1208874a.html

Oncogene (2005) 24, 7180–7189. doi:10.1038/sj.onc.1208874; published online 11 July 2005

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

http://www.clearviewcancer.com/index.php/newswire/details/542  Clearview Cancer Institute  

Gene maps to transform scientists' work on cancer  

The studies by international scientists and Britain's Wellcome Trust Sanger Institute are the first comprehensive descriptions of tumour cell mutations and lay bare all the genetic changes behind melanoma skin cancer and lung cancer.

AND FINALLY, IODINE DO INDEED CURE SKIN CANCER AS ADVOCATED BY DR. SIMONCINI, so keep your hopes intact, keep an open mind and do your own research. I have given you just a little bit of what is available out there without really getting into what is known as "Alternative Treatments" or "Natural Treatments".

Meanwhile read this blog, one just like yours here, written by those who has been there helping those who just ventured into the skin cancer world and see how they CURED their cancer for good:

http://www.topicalinfo.org/forum/topic.asp?TOPIC_ID=409

I am pasting just a small part of the blog below.. Click the link and read the whole thing and see for yourself. Remember the mind, like a parachute functions only when open!

As I said on the start, when it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire at the same time.

With my best to you all,

Dennis (malenomabegone)

I am moved that you are all concern about my well being and me treatment myself as opposed to quickly surgically removing it. I understand that in your opinion quickly surgically excising it is the best option and I respect that. I am taken by your caring and your support for each other. I joined and posted hoping to let you all know that there is another way, not necessarily as an alternative but as an additional to the traditional.

One replied "I have just read thru the links you posted.  I find that quack-science.  You need more than iodine to cure cancer.  It is insulting to people fighting the cancer fight to declare that "cancer is curable" in a blanket statement like that, and if they are not using your bogus methods then they will lose their fight." 

I would like to address this reply and kind of thinking. What I have presented is not "quack-science" just because "main stream medicine" and yourself do not believe in it's cancer curing ability.  The last thing I want is to be "insulting to people fighting the cancer fight".  However cancer IS curable. (See below.) There are numerous ways to fight cancer and nowhere in my previous post did I ever said that "if they are not using your [my] bogus methods then they will lose their fight" When it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire. I am sorry I made you so angry.

My treatment is based on what is advocated by Dr. Simoncini and Dr. Sircus with additions using what other resources I have at my disposal. It works because sodium bicarbonate is a natural substance produced by the body, the maple syrup (sugar) is for the cancer cells as a Trojan Horse to get the sodium bicarbonate into the cancer cells and the iodine is a topical attack from the surface in. Without sodium bicarbonate you will die. It is used in emergency rooms, resuscitations, cases of acidosis, as well as with chemo therapy so they do not poison the whole patient. Not enough bicarbonate leads to diseases and illnesses ultimately to cancer. Remember that the mind, like a parachute functions only when opened.

You can read them here:

Dr. Simoncini:  http://www.curenaturalicancro.com/index.php

http://www.youtube.com/watch?v=npgyZMaewuE&feature  

Sodium bicarbonate, a natural way to treat the cancer

http://www.imva.info/news/sodium-bicarbonate-baking-soda-cancer-treatment.html

and

http://publications.imva.info/index.php/e-books/sodium-bicarbonate-rich-man-s-poor-man-s-cancer-treatment-e-book.html

I joined this blog to learn from you all with an open mind as well as I hope to contribute back by posting additional modalities of treatment SUCH THAT THE CANCER DOES NOT COME BACK. One just posted that after years of having his/her melanoma removed that a new one came up RIGHT WHERE THE ORIGINAL WAS. What a shame that this has to happen. 

I will first supply some of the information I have on melanoma (in no particular order) and end with how (skin) cancer can be beaten. I apologize that it is going to be long and I hope that for those with an open mind  and want to know as much as possible so you can make a truly informed decision that they find at least some of the following research beneficial. Most are on melanoma while others are to show that cancer CAN indeed be beaten so as not to give up hope. Still others are on what influences the development or prevention of cancer that you yourself can take a proactive role for your own health. For those who do not have the time you may wish to just scan the web sites above of Dr. Simoncini and Dr. Sircus or scroll to the bottom to see the effective treatment of Dr. Simoncini put into practice (and YES) curing skin cancer. Cancer CAN be beaten. It happens everyday.

http://informahealthcare.com/doi/abs/10.1080/13590840802305423

Pharmacokinetics of oral vitamin C

Journal of Nutritional and Environmental Medicine

2008, Vol. 17, No. 3 , Pages 169-177

To determine whether plasma levels above 280 µm L⁻¹, which have selectively killed cancer, bacteria or viruses (in laboratory experiments), can be achieved using oral doses of vitamin C.these information beneficial, which is my purpose in joining this blog, to contribute and to learn in return.

http://oncologystat.com/news/Multiple_Melanomas_in_the_Same_Patient_a_Real_Phenomenon_US.html  Multiple Melanomas in the Same Patient a Real Phenomenon

The chances of a patient's developing multiple primary melanomas over a lifetime is a real phenomenon, with an incidence ranging from 2% to 8% among patients who have had a first melanoma, or an average of about 5%.

Of patients who develop additional melanomas, about 80% develop one in addition to the original, 15% develop two, and the remainder develop three or more. "In my practice I have about four people I follow who have had five or six primary melanomas," said Dr. Burrows, who has practiced dermatology for nearly 40 years and is currently with the division of dermatology at Scripps Clinic Rancho Bernardo in San Diego.

http://oncologystat.com/journals/review_articles/YCTRV/Methods_of_detection_of_circulating_melanoma_cells_A_comparative_overview.html

Methods of detection of circulating melanoma cells: A comparative overview

Cancer Treat Rev. 2011 Jun;37(4):284-290, Andrianos Nezos, Pavlos Msaouel, Nikolaos Pissimissis, Peter Lembessis, Antigone Sourla, Athanasios Armakolas, Helen Gogas, Alexandros J. Stratigos, Andreas D. Katsambas, Michael Koutsilieris

Abstract

Disease dissemination is the major cause of melanoma-related death. A crucial step in the metastatic process is the intravascular invasion and circulation of melanoma cells in the bloodstream with subsequent development of distant micrometastases that is initially clinically undetectable and will eventually progress into clinically apparent metastasis. Therefore, the use of molecular methods to detect circulating melanoma cells may be of value in risk stratification and clinical management of such patients. Herein, we review the currently applied techniques for the detection, isolation, enrichment and further characterization of circulating melanoma cells from peripheral blood samples in melanoma patients. Furthermore, we provide a brief overview of the various molecular markers currently being evaluated as prognostic indicators of melanoma progression.

http://oncologystat.com/journals/review_articles/AEP/Vitamin_D_and_Melanoma.html

Vitamin D and Melanoma

Ann Epidemiol. 2009 Jul;19(7):455-461, Kathleen M. Egan

Abstract

Purpose

Ultraviolet light from sunlight and other sources is the major environmental risk factor for melanoma of the skin. Humans also derive most of their vitamin D from exposure to sunlight. This article reviews current evidence that vitamin D might play a preventive role in the development of melanoma or affect tumor aggressiveness or melanoma patient outcomes.

Methods

Literature review.

Results

The vitamin D receptor has been identified in normal melanocytes as well as melanoma cell lines and primary tissue. A few studies have demonstrated relationships of functional polymorphisms in the vitamin D receptor with melanoma risk or tumor aggressiveness. Identifying an independent influence of vitamin D on melanoma risk is hampered by overwhelming confounding by the carcinogenic influence of ultraviolet radiation on skin melanocytes. Nonetheless an inverse association was suggested in a few studies with greater consumption of dairy foods or other dietary sources. Several lines of evidence are consistent with a potential influence for vitamin D on site-specific aggressiveness of skin melanomas, therapeutic response or patient survival.

Conclusion

Additional research is needed to determine whether vitamin D may have a preventive role in melanoma incidence or a salutary influence on melanoma patient outcome.

http://www.youtube.com/watch?v=KOUR9JSmY3w&feature

Connection with Vitamin D and Cancer

http://articles.mercola.com/sites/articles/archive/2011/11/20/deadly-melanoma-not-due-vitamin-d-deficiency.aspx

The Surprising Cause of Melanoma (And No, it's Not Too Much Sun) Posted By Dr. Mercola | November 20 2011 

http://mercola.fileburst.com/PDF/ExpertInterviewTranscripts/InterviewCaroleBaggerlyVitaminD.pdf

A Special Interview with Carole Baggerly  By Dr. Mercola on Vitamin D and Cancer

http://oncologystat.com/journals/review_articles/SOC/Surgical_Approach_to_Primary_Cutaneous_Melanoma.html

Surgical Approach to Primary Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):39-56, Patrick A. Ott, Russell S. Berman

Abstract

The surgical management of primary cutaneous melanoma, from the diagnostic biopsy through the wide local excision and nodal staging, must be carefully planned, and the biology of the melanoma, microstaging and primary tumor pathologic features of the melanoma, location on the body, patient preferences, and comorbidities must be considered. The treating surgeon must balance preservation of oncologic principles, with optimization of functional and aesthetic outcome. This article reviews the rationale behind the surgical approach in the patient with a primary melanoma.

http://oncologystat.com/journals/ew/YSDIA/Falsepositive_cells_in_sentinel_lymph_nodes.html

False-positive cells in sentinel lymph nodes

Semin Diagn Pathol. 2008 May;25(2):116-119, Jeoffry B. Brennick, Shaofeng Yan

Melanoma sentinel lymph nodes (SLN) are carefully evaluated to maximize sensitivity. Examination includes hematoxylin and eosin (H+E) stained sections at multiple levels through the node, with subsequent immunohistochemical (IHC) stains for melanocytic markers if H+E sections are negative for melanoma. However, not all IHC-positive cells in SLN are metastatic melanoma, as evidenced by the presence of MART-1 positive cells in SLN from breast cancer patients with no history of melanoma (so-called ‘false-positive’ cells). These ‘false-positive cells’ could be nodal nevus, non-melanocytic cells with cross-reacting antigenic determinants, phagocytic cells containing melanocyte antigens, or possibly melanocytes or melanocyte stem cells liberated at the time of biopsy of the cutaneous melanoma. Examination of SLN requires careful correlation of H+E and IHC findings.

http://oncologystat.com/journals/review_articles/SOC/Staging_and_Prognosis_of_Cutaneous_Melanoma.html

Staging and Prognosis of Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):1-17, Paxton V. Dickson, Jeffrey E. Gershenwald

Abstract

Staging of cutaneous melanoma continues to evolve through identification and rigorous analysis of potential prognostic factors. In 1998, the American Joint Committee on Cancer (AJCC) Melanoma Staging Committee developed the AJCC melanoma staging database, an international integrated compilation of prospectively accumulated melanoma outcome data from several centers and clinical trial cooperative groups. Analysis of this database resulted in major revisions to the TNM staging system reflected in the sixth edition of the AJCC Cancer Staging Manual published in 2002. More recently, the committee's analysis of an updated melanoma staging database, including prospective data on more than 50,000 patients, led to staging revisions adopted in the seventh edition of the AJCC Cancer Staging Manual published in 2009. This article highlights these revisions, reviews relevant prognostic factors and their impact on staging, and discusses emerging tools that will likely affect future staging systems and clinical practice.

http://oncologystat.com/journals/review_articles/SOC/EvidenceBased_Followup_for_the_Patient_with_Melanoma.html

Evidence-Based Follow-up for the Patient with Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):181-200, Ryan C. Fields, Daniel G. Coit

Abstract

This article reviews the best evidence available to guide the follow-up of patients with melanoma, focusing on incidence of, and detection of, melanoma recurrence, frequency of follow-up visits, yield of, laboratory and radiographic tests, outcomes of patients with recurrent melanoma based on method of detection, detection of secondary melanomas, and stage-specific follow-up.

http://www.surgonc.theclinics.com/article/S1055-3207(10)00091-8/ppt

Immunotherapy of Melanoma: An Update

·       Jade Homsi, MD, Joshua C. Grimm, BA, Patrick Hwu, MD

     The incidence of melanoma has been increasing worldwide. A relationship between melanoma and the immune system was established years ago. Modulating the immune system in the management of different stages of melanoma has been the focus of numerous large randomized trials worldwide. This article reviews the current status of immunotherapy for melanoma, with a focus on the recent promising results from using vaccines, cytotoxic T-lymphocyte antigen-4 (CTLA-4) antibodies, and adoptive cell therapy.

http://www.ncbi.nlm.nih.gov/pubmed/18022553

Surg Oncol Clin N Am. 2007 Oct;16(4):945-73, xi.

Current immunotherapeutic strategies in malignant melanoma.

Agostino NM, Ali A, Nair SG, Mosca PJ.

Source

Department of Internal Medicine, Lehigh Valley Hospital and Health Network, 1240 South Cedar Crest Boulevard, Allentown, PA 18103, USA.

Abstract

The basis of immunotherapy for melanoma is the existence of melanoma-associated antigens that can be targeted by the immune system. Identification of many of these antigens has enabled investigators to develop a wide array of immunotherapy strategies for the treatment of melanoma. Although several of these strategies have been shown to induce antitumor immune responses in some patients, robust clinical responses have been observed less frequently. With exciting recent advancements in this field, however, there is promise of generating potent immunologic responses and translating them more consistently into durable clinical responses. This article reviews several current approaches to immunotherapy for melanoma and describes the key role that surgeons play in advancing this area of oncology.

http://www.oncologystat.com/journals/journal_scans/Ulceration_and_Stage_Are_Predictive_of_Interferon_Efficacy_In_Melanoma_Results_of_the_Phase_III_Adjuvant_Trials_EORTC_18952_and_EORTC_18991.html 

Ulceration and Stage Are Predictive of Interferon Efficacy In Melanoma: Results of the Phase III Adjuvant Trials EORTC 18952 and EORTC 18991

Breast. 2011 Oct 1;20(3), AMM Eggermont, S Suciu, A Testori, A Spatz, et al

TAKE-HOME MESSAGE

This combined analysis of two large prospective trials of adjuvant interferon for treatment of patients with resected melanoma demonstrated that tumor stage and ulceration predict for immunotherapy benefit.

Abstract

Summary: Adjuvant interferon has modest activity in melanoma patients at high risk for relapse. Patient selection is important; stage and ulceration of the primary tumour are key prognostic factors.

Methods: In this post hoc meta-analysis of European Organisation for Research and Treatment of Cancer (EORTC) trials 18952 (intermediate doses of interferon α-2b [IFN] versus observation in stage IIb-III patients) and 18991 (pegylated [PEG]-IFN versus observation in stage III patients), the predictive value of ulceration on the efficacy of IFN/PEG-IFN with regard to relapse-free survival (RFS), distant metastasis-free survival (DMFS), and overall survival (OS) was assessed in the overall population and in subgroups stratified by stage (IIb and III-N1 [microscopic nodal disease] and III-N2 [macroscopic nodal disease]).

Findings: In the overall population, the comparison of IFN/PEG-IFN versus observation for RFS, DMFS and OS yielded estimated hazard ratios (HR) of 0.85 (p=0.004), 0.89 (p=0.04) and 0.94 (p=0.36), respectively. The impact of treatment was greater in the ulceration group (n=849) compared with the non-ulceration group (n=1336) for RFS (test for interaction: p=0.02), DMFS (p<0.001) and OS (p<0.001). The greatest risk reductions were observed in patients with ulceration and stage IIb/III-N1, with estimated HR for RFS, DMFS, and OS of 0.69 (p=0.003), 0.59 (p<0.0001) and 0.58 (p<0.0001), respectively. The efficacy of IFN/PEG-IFN was lower in stage III-N2 patients with ulceration and uniformly absent in patients without ulceration. There was consistency between the data of both trials.

Interpretation: This meta-analysis of the EORTC 18952 and 18991 trials indicated that both tumour stage and ulceration were predictive factors for the efficacy of adjuvant IFN/PEG-IFN therapy.

http://oncologystat.com/journals/review_articles/archive/Metastatic_Melanoma_An_AJCC_Review.html

or  

http://www.communityoncology.net/co/journal/articles/0508441.pdf

Metastatic Melanoma: An AJCC Review

Community Oncology. 2008 Aug 1;5(8):441-445, SS Agarwala

Abstract

Outside clinical trials, current therapeutic options for patients with metastatic melanoma appear to be of limited benefit. Combination chemotherapy has not been shown to improve outcomes over single-agent chemotherapy, and dacarbazine, which is still the only agent approved by the US Food and Drug Administration for this disease, has produced low response rates and little meaningful improvement in survival. However, with the development and testing of several new compounds, both in the area of immunotherapy and targeted therapy, the future for patients with this disease may become brighter.

News Story: Investigational TKI Active Against Advanced Melanoma in Early Trial »

News Story: Tremelimumab Monotherapy Adds No Benefit Over Chemo in Metastatic Melanoma »

Journal Article: Treatment of Metastatic Melanoma With Autologous CD4+ T Cells Against NY-ESO-1 »

Journal Article: Biochemotherapy for the Treatment of Metastatic Malignant Melanoma: A Systematic Review »

Journal Article: Treatments for Metastatic Melanoma: Synthesis of Evidence From Randomized Trials »

Journal Article: Chemotherapy Compared With Biochemotherapy for the Treatment of Metastatic Melanoma: A Meta-analysis of 18 Trials Involving 2,621 Patients »

http://oncologystat.com/journals/review_articles/HOC/Progress_in_Melanoma_Histopathology_and_Diagnosis.html

Progress in Melanoma Histopathology and Diagnosis

Hematol Oncol Clin North Am. 2009 Jun;23(3):467-480, Adriano Piris, Martin C. Mihm

Abstract

The past 15 years have seen rapid advances in both our understanding of hereditary melanoma genetics and the technologies that enable scientists to make discoveries. Despite great efforts by many groups worldwide, other high-risk melanoma loci besides CDKN2A still remain elusive. A panel of polymorphisms that appears to confer low-to-moderate risk for melanoma has been assembled through functional and genome-wide association studies. The goal of personalized melanoma risk prediction is within our reach, although true clinical use has yet to be established.

http://oncologystat.com/news/Melanoma_Field_Cells_May_Explain_Local_Tumor_Recurrence_US.html  Melanoma Field Cells May Explain Local Tumor Recurrence

Elsevier Global Medical News. 2009 Mar 2, B Jancin  MAUI, HAWAII (EGMN) – The recent discovery of an entity called melanoma field cells that are often present in seemingly normal skin surrounding primary melanomas could ultimately force an overhaul of standard recommended excision margins.

These melanoma field cells are morphologically normal junctional melanocytes and thus cannot be identified using histopathologic criteria. Yet they are genetically melanoma as demonstrated using comparative genomic hybridization and fluorescent in situ hybridization, Dr. Maxwell A. Fung explained at the annual Hawaii Dermatology Seminar sponsored by the Skin Disease Education Foundation.

http://ebm.rsmjournals.com/content/234/8/825.full.pdf+html?sid=658bdab7-e25a-4654-bb4c-ac0d3900cbda

Experimental Biology and Medicine

Molecular Targets of Nutraceuticals Derived from Dietary Spices: Potential Role in Suppression of Inflammation and Tumorigenesis

Overall our review suggests “adding spice to your life” may serve as a healthy and delicious way to ward off cancer and other chronic diseases.

http://journals.lww.com/melanomaresearch/Abstract/2007/10000/Curcumin_downregulates_the_constitutive_activity.2.aspx

Melanoma Research:

October 2007 – Volume 17 – Issue 5 – pp 274-283

doi: 10.1097/CMR.0b013e3282ed3d0e

Original Articles

Curcumin downregulates the constitutive activity of NF-[kappa]B and induces apoptosis in novel mouse melanoma cells

Abstract

Melanoma, the most deadly form of skin cancer, is very aggressive and resistant to present therapies. The transcription factor nuclear factor-kappa B (NF-κB) has been reported to be constitutively active in many types of cancer. Constitutively active NF-κB seen in melanoma likely plays a central role in cell survival and growth. We have established and characterized novel cell lines from our murine melanoma model. Here we report the constitutive activity of NF-κB in these melanoma-derived cells, as shown by electrophoretic mobility shift assay and reporter assays. We hypothesized that agents that inhibit NF-κB may also inhibit cell proliferation and may induce apoptosis in such melanoma cells. Curcumin has been shown to inhibit NF-κB activity in several cell types. In our system, curcumin selectively inhibited growth of melanoma cells, but not normal melanocytes. Curcumin induced melanoma cells to undergo apoptosis, as shown by caspase-3 activation, inversion of membrane phosphatidyl serine, and increases in cells in the sub-G₁ phase. A curcumin dose-dependent inhibition of NF-κB-driven reporter activity correlated with decreased levels of phospho-IκBα, and decreased expression of NF-κB-target genes COX-2 and cyclin D1. This study demonstrates that the use of cells from our model system can facilitate studies of signaling pathways in melanoma. We furthermore conclude that curcumin, a natural and safe compound, inhibits NF-κB activity and the expression of its downstream target genes, and also selectively induces apoptosis of melanoma cells but not normal melanocytes. These encouraging in-vitro results support further investigation of curcumin for treatment of melanoma in vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12680238

Anticancer Res. 2003 Jan-Feb;23(1A):363-98.

Anticancer potential of curcumin: preclinical and clinical studies.

Aggarwal BB, Kumar A, Bharti AC.

Cytokine Research Section, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX, USA. [email protected]

Abstract

Curcumin (diferuloylmethane) is a polyphenol derived from the plant Curcuma longa, commonly called turmeric. Extensive research over the last 50 years has indicated this polyphenol can both prevent and treat cancer. The anticancer potential of curcumin stems from its ability to suppress proliferation of a wide variety of tumor cells, down-regulate transcription factors NF-kappa B, AP-1 and Egr-1; down-regulate the expression of COX2, LOX, NOS, MMP-9, uPA, TNF, chemokines, cell surface adhesion molecules and cyclin D1; down-regulate growth factor receptors (such as EGFR and HER2); and inhibit the activity of c-Jun N-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases. In several systems, curcumin has been described as a potent antioxidant and anti-inflammatory agent. Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis. Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day. All of these studies suggest that curcumin has enormous potential in the prevention and therapy of cancer. The current review describes in detail the data supporting these studies.

http://www.experts.scival.com/wayne/pubDetail.asp?t=pm&id=15252141&amp;

Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation.

http://ur.rutgers.edu/medrel/viewArticle.html?ArticleID=49

 Rutgers, The State University of New Jersey: Curry and Cauliflower Could Halt Prostate Cancer

http://www.jcrows.com/curryfightsprostatecancer.html  

Curry fights prostate cancer, study finds

http://mss3.libraries.rutgers.edu/dlr/showfed.php?pid=rutgers-lib:25088  

Prostate cancer chemoprevention by dietary phytochemicals: 

Chemoprevention entails the use of preferably dietary agents to block or suppress the various stages of prostate carcinogenesis. Flavonoids, the essential components of fruits and vegetables can modulate transcription factor AP-1 and its upstream signaling cascades mainly ERK-MAPK and JNK-MAPK in human androgen insensitive prostate cancer (PC3) cells. Soy isoflavone concentrate can upregulate the expression of several phase II detoxifying and antioxidant genes in an NF-E2-related factor 2 (Nrf2) dependent manner. In addition to detoxifying genes, soy isoflavone concentrate can also modulate the expression of genes such as LATS2, GREB1, calpain and many more in an Nrf2 dependent manner. 

In one such transgenic model, curcumin or PEITC suppressed high grade PIN levels. However a combination of low doses of these agents worked remarkably well in suppressing tumors all together.

http://www.newswise.com/articles/view/573327/

Genetic Evidence That Antioxidants Can Help Treat Cancer  

“Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth,” said lead researcher Michael P. Lisanti, M.D., Ph.D., professor of cancer biology at Jefferson Medical College of Thomas Jefferson University and member of the Kimmel Cancer Center at Jefferson. “This means we need to make anti-cancer drugs that specially target this type of oxidative stress. And there are already antioxidant drugs out there on the market as dietary supplements, like N-acetyl cysteine.” 

The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.

“Antioxidants have been associated with cancer reducing effects—beta carotene, for example—but the mechanisms, the genetic evidence, has been lacking,” Dr. Lisanti said. “This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth.”

 These findings were originally published in the online February 15 issue of Cancer Biology & Therapy.

http://cancerres.aacrjournals.org/content/71/13/4484

A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.

http://www.newswise.com/articles/view/574151/?sc=mwhn

Biologists Show How Veggies Work in Cancer-Fighting Diet

Released: 3/7/2011 3:00 PM EST 

Source: University of Alabama at Birmingham

Newswise — BIRMINGHAM, Ala. – Mothers around the world now collectively can say, “I told you so.”

Your vegetables are good for you, says a research review published by scientists from the University of Alabama at Birmingham in the journal Clinical Epigenetics.

In particular, vegetables such as broccoli and cabbage are filled with compounds that could help reverse or prevent cancers and other aging-related diseases as part of the “epigenetics diet,” a new lifestyle concept coined after the article’s publication.

“Your mother always told you to eat your vegetables, and she was right,” says co-author Trygve Tollefsbol, Ph.D., D.O., a biology professor in the UAB College of Arts and Sciences. “But now we better understand why she was right — compounds in many of these foods suppress gene aberrations that over time cause fatal diseases.”

Epigenetics is the study of the changes in human gene expressions with time, changes that can cause cancer and Alzheimer’s, among other diseases. In recent years, epigenetics research worldwide, including numerous studies conducted at UAB, have identified specific food compounds that inhibit negative epigenetic effects.

Those foods include soybeans, cauliflower, broccoli and cabbage. Green tea, fava beans, kale, grapes and the spice turmeric round out the diet.

“The epigenetics diet can be adopted easily, because the concentrations of the compounds needed for a positive effect are readily achievable,” says lead author Syed Meeran, Ph.D., a research assistant professor in Tollefsbol’s UAB Department of Biology laboratory.

For example, Meeran says sipping tea compounds called polyphenols in daily amounts that are equivalent to approximately three cups of green tea has been shown to reverse breast cancer in laboratory mice by suppressing the gene that triggers the disease. Similarly, a daily cup of broccoli sprouts, which has sulforaphane as an active compound, has been shown to reduce the risk of developing many cancers.

“Our review article has drawn everything together from global studies, and the common theme is that compounds in the epigenetics diet foods can, at the very least, help us lead healthier lives and help our bodies prevent potentially debilitating diseases like breast cancer and Alzheimer’s,” Tollefsbol says.

http://www.nature.com/onc/journal/v24/n48/abs/1208874a.html

Oncogene (2005) 24, 7180–7189. doi:10.1038/sj.onc.1208874; published online 11 July 2005

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

http://www.clearviewcancer.com/index.php/newswire/details/542  Clearview Cancer Institute  

Gene maps to transform scientists' work on cancer  

The studies by international scientists and Britain's Wellcome Trust Sanger Institute are the first comprehensive descriptions of tumour cell mutations and lay bare all the genetic changes behind melanoma skin cancer and lung cancer.

AND FINALLY, IODINE DO INDEED CURE SKIN CANCER AS ADVOCATED BY DR. SIMONCINI, so keep your hopes intact, keep an open mind and do your own research. I have given you just a little bit of what is available out there without really getting into what is known as "Alternative Treatments" or "Natural Treatments".

Meanwhile read this blog, one just like yours here, written by those who has been there helping those who just ventured into the skin cancer world and see how they CURED their cancer for good:

http://www.topicalinfo.org/forum/topic.asp?TOPIC_ID=409

I am pasting just a small part of the blog below.. Click the link and read the whole thing and see for yourself. Remember the mind, like a parachute functions only when open!

As I said on the start, when it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire at the same time.

With my best to you all,

Dennis (malenomabegone)

I am moved that you are all concern about my well being and me treatment myself as opposed to quickly surgically removing it. I understand that in your opinion quickly surgically excising it is the best option and I respect that. I am taken by your caring and your support for each other. I joined and posted hoping to let you all know that there is another way, not necessarily as an alternative but as an additional to the traditional.

One replied "I have just read thru the links you posted.  I find that quack-science.  You need more than iodine to cure cancer.  It is insulting to people fighting the cancer fight to declare that "cancer is curable" in a blanket statement like that, and if they are not using your bogus methods then they will lose their fight." 

I would like to address this reply and kind of thinking. What I have presented is not "quack-science" just because "main stream medicine" and yourself do not believe in it's cancer curing ability.  The last thing I want is to be "insulting to people fighting the cancer fight".  However cancer IS curable. (See below.) There are numerous ways to fight cancer and nowhere in my previous post did I ever said that "if they are not using your [my] bogus methods then they will lose their fight" When it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire. I am sorry I made you so angry.

My treatment is based on what is advocated by Dr. Simoncini and Dr. Sircus with additions using what other resources I have at my disposal. It works because sodium bicarbonate is a natural substance produced by the body, the maple syrup (sugar) is for the cancer cells as a Trojan Horse to get the sodium bicarbonate into the cancer cells and the iodine is a topical attack from the surface in. Without sodium bicarbonate you will die. It is used in emergency rooms, resuscitations, cases of acidosis, as well as with chemo therapy so they do not poison the whole patient. Not enough bicarbonate leads to diseases and illnesses ultimately to cancer. Remember that the mind, like a parachute functions only when opened.

You can read them here:

Dr. Simoncini:  http://www.curenaturalicancro.com/index.php

http://www.youtube.com/watch?v=npgyZMaewuE&feature  

Sodium bicarbonate, a natural way to treat the cancer

http://www.imva.info/news/sodium-bicarbonate-baking-soda-cancer-treatment.html

and

http://publications.imva.info/index.php/e-books/sodium-bicarbonate-rich-man-s-poor-man-s-cancer-treatment-e-book.html

I joined this blog to learn from you all with an open mind as well as I hope to contribute back by posting additional modalities of treatment SUCH THAT THE CANCER DOES NOT COME BACK. One just posted that after years of having his/her melanoma removed that a new one came up RIGHT WHERE THE ORIGINAL WAS. What a shame that this has to happen. 

I will first supply some of the information I have on melanoma (in no particular order) and end with how (skin) cancer can be beaten. I apologize that it is going to be long and I hope that for those with an open mind  and want to know as much as possible so you can make a truly informed decision that they find at least some of the following research beneficial. Most are on melanoma while others are to show that cancer CAN indeed be beaten so as not to give up hope. Still others are on what influences the development or prevention of cancer that you yourself can take a proactive role for your own health. For those who do not have the time you may wish to just scan the web sites above of Dr. Simoncini and Dr. Sircus or scroll to the bottom to see the effective treatment of Dr. Simoncini put into practice (and YES) curing skin cancer. Cancer CAN be beaten. It happens everyday.

http://informahealthcare.com/doi/abs/10.1080/13590840802305423

Pharmacokinetics of oral vitamin C

Journal of Nutritional and Environmental Medicine

2008, Vol. 17, No. 3 , Pages 169-177

To determine whether plasma levels above 280 µm L⁻¹, which have selectively killed cancer, bacteria or viruses (in laboratory experiments), can be achieved using oral doses of vitamin C.these information beneficial, which is my purpose in joining this blog, to contribute and to learn in return.

http://oncologystat.com/news/Multiple_Melanomas_in_the_Same_Patient_a_Real_Phenomenon_US.html  Multiple Melanomas in the Same Patient a Real Phenomenon

The chances of a patient's developing multiple primary melanomas over a lifetime is a real phenomenon, with an incidence ranging from 2% to 8% among patients who have had a first melanoma, or an average of about 5%.

Of patients who develop additional melanomas, about 80% develop one in addition to the original, 15% develop two, and the remainder develop three or more. "In my practice I have about four people I follow who have had five or six primary melanomas," said Dr. Burrows, who has practiced dermatology for nearly 40 years and is currently with the division of dermatology at Scripps Clinic Rancho Bernardo in San Diego.

http://oncologystat.com/journals/review_articles/YCTRV/Methods_of_detection_of_circulating_melanoma_cells_A_comparative_overview.html

Methods of detection of circulating melanoma cells: A comparative overview

Cancer Treat Rev. 2011 Jun;37(4):284-290, Andrianos Nezos, Pavlos Msaouel, Nikolaos Pissimissis, Peter Lembessis, Antigone Sourla, Athanasios Armakolas, Helen Gogas, Alexandros J. Stratigos, Andreas D. Katsambas, Michael Koutsilieris

Abstract

Disease dissemination is the major cause of melanoma-related death. A crucial step in the metastatic process is the intravascular invasion and circulation of melanoma cells in the bloodstream with subsequent development of distant micrometastases that is initially clinically undetectable and will eventually progress into clinically apparent metastasis. Therefore, the use of molecular methods to detect circulating melanoma cells may be of value in risk stratification and clinical management of such patients. Herein, we review the currently applied techniques for the detection, isolation, enrichment and further characterization of circulating melanoma cells from peripheral blood samples in melanoma patients. Furthermore, we provide a brief overview of the various molecular markers currently being evaluated as prognostic indicators of melanoma progression.

http://oncologystat.com/journals/review_articles/AEP/Vitamin_D_and_Melanoma.html

Vitamin D and Melanoma

Ann Epidemiol. 2009 Jul;19(7):455-461, Kathleen M. Egan

Abstract

Purpose

Ultraviolet light from sunlight and other sources is the major environmental risk factor for melanoma of the skin. Humans also derive most of their vitamin D from exposure to sunlight. This article reviews current evidence that vitamin D might play a preventive role in the development of melanoma or affect tumor aggressiveness or melanoma patient outcomes.

Methods

Literature review.

Results

The vitamin D receptor has been identified in normal melanocytes as well as melanoma cell lines and primary tissue. A few studies have demonstrated relationships of functional polymorphisms in the vitamin D receptor with melanoma risk or tumor aggressiveness. Identifying an independent influence of vitamin D on melanoma risk is hampered by overwhelming confounding by the carcinogenic influence of ultraviolet radiation on skin melanocytes. Nonetheless an inverse association was suggested in a few studies with greater consumption of dairy foods or other dietary sources. Several lines of evidence are consistent with a potential influence for vitamin D on site-specific aggressiveness of skin melanomas, therapeutic response or patient survival.

Conclusion

Additional research is needed to determine whether vitamin D may have a preventive role in melanoma incidence or a salutary influence on melanoma patient outcome.

http://www.youtube.com/watch?v=KOUR9JSmY3w&feature

Connection with Vitamin D and Cancer

http://articles.mercola.com/sites/articles/archive/2011/11/20/deadly-melanoma-not-due-vitamin-d-deficiency.aspx

The Surprising Cause of Melanoma (And No, it's Not Too Much Sun) Posted By Dr. Mercola | November 20 2011 

http://mercola.fileburst.com/PDF/ExpertInterviewTranscripts/InterviewCaroleBaggerlyVitaminD.pdf

A Special Interview with Carole Baggerly  By Dr. Mercola on Vitamin D and Cancer

http://oncologystat.com/journals/review_articles/SOC/Surgical_Approach_to_Primary_Cutaneous_Melanoma.html

Surgical Approach to Primary Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):39-56, Patrick A. Ott, Russell S. Berman

Abstract

The surgical management of primary cutaneous melanoma, from the diagnostic biopsy through the wide local excision and nodal staging, must be carefully planned, and the biology of the melanoma, microstaging and primary tumor pathologic features of the melanoma, location on the body, patient preferences, and comorbidities must be considered. The treating surgeon must balance preservation of oncologic principles, with optimization of functional and aesthetic outcome. This article reviews the rationale behind the surgical approach in the patient with a primary melanoma.

http://oncologystat.com/journals/ew/YSDIA/Falsepositive_cells_in_sentinel_lymph_nodes.html

False-positive cells in sentinel lymph nodes

Semin Diagn Pathol. 2008 May;25(2):116-119, Jeoffry B. Brennick, Shaofeng Yan

Melanoma sentinel lymph nodes (SLN) are carefully evaluated to maximize sensitivity. Examination includes hematoxylin and eosin (H+E) stained sections at multiple levels through the node, with subsequent immunohistochemical (IHC) stains for melanocytic markers if H+E sections are negative for melanoma. However, not all IHC-positive cells in SLN are metastatic melanoma, as evidenced by the presence of MART-1 positive cells in SLN from breast cancer patients with no history of melanoma (so-called ‘false-positive’ cells). These ‘false-positive cells’ could be nodal nevus, non-melanocytic cells with cross-reacting antigenic determinants, phagocytic cells containing melanocyte antigens, or possibly melanocytes or melanocyte stem cells liberated at the time of biopsy of the cutaneous melanoma. Examination of SLN requires careful correlation of H+E and IHC findings.

http://oncologystat.com/journals/review_articles/SOC/Staging_and_Prognosis_of_Cutaneous_Melanoma.html

Staging and Prognosis of Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):1-17, Paxton V. Dickson, Jeffrey E. Gershenwald

Abstract

Staging of cutaneous melanoma continues to evolve through identification and rigorous analysis of potential prognostic factors. In 1998, the American Joint Committee on Cancer (AJCC) Melanoma Staging Committee developed the AJCC melanoma staging database, an international integrated compilation of prospectively accumulated melanoma outcome data from several centers and clinical trial cooperative groups. Analysis of this database resulted in major revisions to the TNM staging system reflected in the sixth edition of the AJCC Cancer Staging Manual published in 2002. More recently, the committee's analysis of an updated melanoma staging database, including prospective data on more than 50,000 patients, led to staging revisions adopted in the seventh edition of the AJCC Cancer Staging Manual published in 2009. This article highlights these revisions, reviews relevant prognostic factors and their impact on staging, and discusses emerging tools that will likely affect future staging systems and clinical practice.

http://oncologystat.com/journals/review_articles/SOC/EvidenceBased_Followup_for_the_Patient_with_Melanoma.html

Evidence-Based Follow-up for the Patient with Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):181-200, Ryan C. Fields, Daniel G. Coit

Abstract

This article reviews the best evidence available to guide the follow-up of patients with melanoma, focusing on incidence of, and detection of, melanoma recurrence, frequency of follow-up visits, yield of, laboratory and radiographic tests, outcomes of patients with recurrent melanoma based on method of detection, detection of secondary melanomas, and stage-specific follow-up.

http://www.surgonc.theclinics.com/article/S1055-3207(10)00091-8/ppt

Immunotherapy of Melanoma: An Update

·       Jade Homsi, MD, Joshua C. Grimm, BA, Patrick Hwu, MD

     The incidence of melanoma has been increasing worldwide. A relationship between melanoma and the immune system was established years ago. Modulating the immune system in the management of different stages of melanoma has been the focus of numerous large randomized trials worldwide. This article reviews the current status of immunotherapy for melanoma, with a focus on the recent promising results from using vaccines, cytotoxic T-lymphocyte antigen-4 (CTLA-4) antibodies, and adoptive cell therapy.

http://www.ncbi.nlm.nih.gov/pubmed/18022553

Surg Oncol Clin N Am. 2007 Oct;16(4):945-73, xi.

Current immunotherapeutic strategies in malignant melanoma.

Agostino NM, Ali A, Nair SG, Mosca PJ.

Source

Department of Internal Medicine, Lehigh Valley Hospital and Health Network, 1240 South Cedar Crest Boulevard, Allentown, PA 18103, USA.

Abstract

The basis of immunotherapy for melanoma is the existence of melanoma-associated antigens that can be targeted by the immune system. Identification of many of these antigens has enabled investigators to develop a wide array of immunotherapy strategies for the treatment of melanoma. Although several of these strategies have been shown to induce antitumor immune responses in some patients, robust clinical responses have been observed less frequently. With exciting recent advancements in this field, however, there is promise of generating potent immunologic responses and translating them more consistently into durable clinical responses. This article reviews several current approaches to immunotherapy for melanoma and describes the key role that surgeons play in advancing this area of oncology.

http://www.oncologystat.com/journals/journal_scans/Ulceration_and_Stage_Are_Predictive_of_Interferon_Efficacy_In_Melanoma_Results_of_the_Phase_III_Adjuvant_Trials_EORTC_18952_and_EORTC_18991.html 

Ulceration and Stage Are Predictive of Interferon Efficacy In Melanoma: Results of the Phase III Adjuvant Trials EORTC 18952 and EORTC 18991

Breast. 2011 Oct 1;20(3), AMM Eggermont, S Suciu, A Testori, A Spatz, et al

TAKE-HOME MESSAGE

This combined analysis of two large prospective trials of adjuvant interferon for treatment of patients with resected melanoma demonstrated that tumor stage and ulceration predict for immunotherapy benefit.

Abstract

Summary: Adjuvant interferon has modest activity in melanoma patients at high risk for relapse. Patient selection is important; stage and ulceration of the primary tumour are key prognostic factors.

Methods: In this post hoc meta-analysis of European Organisation for Research and Treatment of Cancer (EORTC) trials 18952 (intermediate doses of interferon α-2b [IFN] versus observation in stage IIb-III patients) and 18991 (pegylated [PEG]-IFN versus observation in stage III patients), the predictive value of ulceration on the efficacy of IFN/PEG-IFN with regard to relapse-free survival (RFS), distant metastasis-free survival (DMFS), and overall survival (OS) was assessed in the overall population and in subgroups stratified by stage (IIb and III-N1 [microscopic nodal disease] and III-N2 [macroscopic nodal disease]).

Findings: In the overall population, the comparison of IFN/PEG-IFN versus observation for RFS, DMFS and OS yielded estimated hazard ratios (HR) of 0.85 (p=0.004), 0.89 (p=0.04) and 0.94 (p=0.36), respectively. The impact of treatment was greater in the ulceration group (n=849) compared with the non-ulceration group (n=1336) for RFS (test for interaction: p=0.02), DMFS (p<0.001) and OS (p<0.001). The greatest risk reductions were observed in patients with ulceration and stage IIb/III-N1, with estimated HR for RFS, DMFS, and OS of 0.69 (p=0.003), 0.59 (p<0.0001) and 0.58 (p<0.0001), respectively. The efficacy of IFN/PEG-IFN was lower in stage III-N2 patients with ulceration and uniformly absent in patients without ulceration. There was consistency between the data of both trials.

Interpretation: This meta-analysis of the EORTC 18952 and 18991 trials indicated that both tumour stage and ulceration were predictive factors for the efficacy of adjuvant IFN/PEG-IFN therapy.

http://oncologystat.com/journals/review_articles/archive/Metastatic_Melanoma_An_AJCC_Review.html

or  

http://www.communityoncology.net/co/journal/articles/0508441.pdf

Metastatic Melanoma: An AJCC Review

Community Oncology. 2008 Aug 1;5(8):441-445, SS Agarwala

Abstract

Outside clinical trials, current therapeutic options for patients with metastatic melanoma appear to be of limited benefit. Combination chemotherapy has not been shown to improve outcomes over single-agent chemotherapy, and dacarbazine, which is still the only agent approved by the US Food and Drug Administration for this disease, has produced low response rates and little meaningful improvement in survival. However, with the development and testing of several new compounds, both in the area of immunotherapy and targeted therapy, the future for patients with this disease may become brighter.

News Story: Investigational TKI Active Against Advanced Melanoma in Early Trial »

News Story: Tremelimumab Monotherapy Adds No Benefit Over Chemo in Metastatic Melanoma »

Journal Article: Treatment of Metastatic Melanoma With Autologous CD4+ T Cells Against NY-ESO-1 »

Journal Article: Biochemotherapy for the Treatment of Metastatic Malignant Melanoma: A Systematic Review »

Journal Article: Treatments for Metastatic Melanoma: Synthesis of Evidence From Randomized Trials »

Journal Article: Chemotherapy Compared With Biochemotherapy for the Treatment of Metastatic Melanoma: A Meta-analysis of 18 Trials Involving 2,621 Patients »

http://oncologystat.com/journals/review_articles/HOC/Progress_in_Melanoma_Histopathology_and_Diagnosis.html

Progress in Melanoma Histopathology and Diagnosis

Hematol Oncol Clin North Am. 2009 Jun;23(3):467-480, Adriano Piris, Martin C. Mihm

Abstract

The past 15 years have seen rapid advances in both our understanding of hereditary melanoma genetics and the technologies that enable scientists to make discoveries. Despite great efforts by many groups worldwide, other high-risk melanoma loci besides CDKN2A still remain elusive. A panel of polymorphisms that appears to confer low-to-moderate risk for melanoma has been assembled through functional and genome-wide association studies. The goal of personalized melanoma risk prediction is within our reach, although true clinical use has yet to be established.

http://oncologystat.com/news/Melanoma_Field_Cells_May_Explain_Local_Tumor_Recurrence_US.html  Melanoma Field Cells May Explain Local Tumor Recurrence

Elsevier Global Medical News. 2009 Mar 2, B Jancin  MAUI, HAWAII (EGMN) – The recent discovery of an entity called melanoma field cells that are often present in seemingly normal skin surrounding primary melanomas could ultimately force an overhaul of standard recommended excision margins.

These melanoma field cells are morphologically normal junctional melanocytes and thus cannot be identified using histopathologic criteria. Yet they are genetically melanoma as demonstrated using comparative genomic hybridization and fluorescent in situ hybridization, Dr. Maxwell A. Fung explained at the annual Hawaii Dermatology Seminar sponsored by the Skin Disease Education Foundation.

http://ebm.rsmjournals.com/content/234/8/825.full.pdf+html?sid=658bdab7-e25a-4654-bb4c-ac0d3900cbda

Experimental Biology and Medicine

Molecular Targets of Nutraceuticals Derived from Dietary Spices: Potential Role in Suppression of Inflammation and Tumorigenesis

Overall our review suggests “adding spice to your life” may serve as a healthy and delicious way to ward off cancer and other chronic diseases.

http://journals.lww.com/melanomaresearch/Abstract/2007/10000/Curcumin_downregulates_the_constitutive_activity.2.aspx

Melanoma Research:

October 2007 – Volume 17 – Issue 5 – pp 274-283

doi: 10.1097/CMR.0b013e3282ed3d0e

Original Articles

Curcumin downregulates the constitutive activity of NF-[kappa]B and induces apoptosis in novel mouse melanoma cells

Abstract

Melanoma, the most deadly form of skin cancer, is very aggressive and resistant to present therapies. The transcription factor nuclear factor-kappa B (NF-κB) has been reported to be constitutively active in many types of cancer. Constitutively active NF-κB seen in melanoma likely plays a central role in cell survival and growth. We have established and characterized novel cell lines from our murine melanoma model. Here we report the constitutive activity of NF-κB in these melanoma-derived cells, as shown by electrophoretic mobility shift assay and reporter assays. We hypothesized that agents that inhibit NF-κB may also inhibit cell proliferation and may induce apoptosis in such melanoma cells. Curcumin has been shown to inhibit NF-κB activity in several cell types. In our system, curcumin selectively inhibited growth of melanoma cells, but not normal melanocytes. Curcumin induced melanoma cells to undergo apoptosis, as shown by caspase-3 activation, inversion of membrane phosphatidyl serine, and increases in cells in the sub-G₁ phase. A curcumin dose-dependent inhibition of NF-κB-driven reporter activity correlated with decreased levels of phospho-IκBα, and decreased expression of NF-κB-target genes COX-2 and cyclin D1. This study demonstrates that the use of cells from our model system can facilitate studies of signaling pathways in melanoma. We furthermore conclude that curcumin, a natural and safe compound, inhibits NF-κB activity and the expression of its downstream target genes, and also selectively induces apoptosis of melanoma cells but not normal melanocytes. These encouraging in-vitro results support further investigation of curcumin for treatment of melanoma in vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12680238

Anticancer Res. 2003 Jan-Feb;23(1A):363-98.

Anticancer potential of curcumin: preclinical and clinical studies.

Aggarwal BB, Kumar A, Bharti AC.

Cytokine Research Section, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX, USA. [email protected]

Abstract

Curcumin (diferuloylmethane) is a polyphenol derived from the plant Curcuma longa, commonly called turmeric. Extensive research over the last 50 years has indicated this polyphenol can both prevent and treat cancer. The anticancer potential of curcumin stems from its ability to suppress proliferation of a wide variety of tumor cells, down-regulate transcription factors NF-kappa B, AP-1 and Egr-1; down-regulate the expression of COX2, LOX, NOS, MMP-9, uPA, TNF, chemokines, cell surface adhesion molecules and cyclin D1; down-regulate growth factor receptors (such as EGFR and HER2); and inhibit the activity of c-Jun N-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases. In several systems, curcumin has been described as a potent antioxidant and anti-inflammatory agent. Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis. Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day. All of these studies suggest that curcumin has enormous potential in the prevention and therapy of cancer. The current review describes in detail the data supporting these studies.

http://www.experts.scival.com/wayne/pubDetail.asp?t=pm&id=15252141&amp;

Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation.

http://ur.rutgers.edu/medrel/viewArticle.html?ArticleID=49

 Rutgers, The State University of New Jersey: Curry and Cauliflower Could Halt Prostate Cancer

http://www.jcrows.com/curryfightsprostatecancer.html  

Curry fights prostate cancer, study finds

http://mss3.libraries.rutgers.edu/dlr/showfed.php?pid=rutgers-lib:25088  

Prostate cancer chemoprevention by dietary phytochemicals: 

Chemoprevention entails the use of preferably dietary agents to block or suppress the various stages of prostate carcinogenesis. Flavonoids, the essential components of fruits and vegetables can modulate transcription factor AP-1 and its upstream signaling cascades mainly ERK-MAPK and JNK-MAPK in human androgen insensitive prostate cancer (PC3) cells. Soy isoflavone concentrate can upregulate the expression of several phase II detoxifying and antioxidant genes in an NF-E2-related factor 2 (Nrf2) dependent manner. In addition to detoxifying genes, soy isoflavone concentrate can also modulate the expression of genes such as LATS2, GREB1, calpain and many more in an Nrf2 dependent manner. 

In one such transgenic model, curcumin or PEITC suppressed high grade PIN levels. However a combination of low doses of these agents worked remarkably well in suppressing tumors all together.

http://www.newswise.com/articles/view/573327/

Genetic Evidence That Antioxidants Can Help Treat Cancer  

“Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth,” said lead researcher Michael P. Lisanti, M.D., Ph.D., professor of cancer biology at Jefferson Medical College of Thomas Jefferson University and member of the Kimmel Cancer Center at Jefferson. “This means we need to make anti-cancer drugs that specially target this type of oxidative stress. And there are already antioxidant drugs out there on the market as dietary supplements, like N-acetyl cysteine.” 

The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.

“Antioxidants have been associated with cancer reducing effects—beta carotene, for example—but the mechanisms, the genetic evidence, has been lacking,” Dr. Lisanti said. “This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth.”

 These findings were originally published in the online February 15 issue of Cancer Biology & Therapy.

http://cancerres.aacrjournals.org/content/71/13/4484

A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.

http://www.newswise.com/articles/view/574151/?sc=mwhn

Biologists Show How Veggies Work in Cancer-Fighting Diet

Released: 3/7/2011 3:00 PM EST 

Source: University of Alabama at Birmingham

Newswise — BIRMINGHAM, Ala. – Mothers around the world now collectively can say, “I told you so.”

Your vegetables are good for you, says a research review published by scientists from the University of Alabama at Birmingham in the journal Clinical Epigenetics.

In particular, vegetables such as broccoli and cabbage are filled with compounds that could help reverse or prevent cancers and other aging-related diseases as part of the “epigenetics diet,” a new lifestyle concept coined after the article’s publication.

“Your mother always told you to eat your vegetables, and she was right,” says co-author Trygve Tollefsbol, Ph.D., D.O., a biology professor in the UAB College of Arts and Sciences. “But now we better understand why she was right — compounds in many of these foods suppress gene aberrations that over time cause fatal diseases.”

Epigenetics is the study of the changes in human gene expressions with time, changes that can cause cancer and Alzheimer’s, among other diseases. In recent years, epigenetics research worldwide, including numerous studies conducted at UAB, have identified specific food compounds that inhibit negative epigenetic effects.

Those foods include soybeans, cauliflower, broccoli and cabbage. Green tea, fava beans, kale, grapes and the spice turmeric round out the diet.

“The epigenetics diet can be adopted easily, because the concentrations of the compounds needed for a positive effect are readily achievable,” says lead author Syed Meeran, Ph.D., a research assistant professor in Tollefsbol’s UAB Department of Biology laboratory.

For example, Meeran says sipping tea compounds called polyphenols in daily amounts that are equivalent to approximately three cups of green tea has been shown to reverse breast cancer in laboratory mice by suppressing the gene that triggers the disease. Similarly, a daily cup of broccoli sprouts, which has sulforaphane as an active compound, has been shown to reduce the risk of developing many cancers.

“Our review article has drawn everything together from global studies, and the common theme is that compounds in the epigenetics diet foods can, at the very least, help us lead healthier lives and help our bodies prevent potentially debilitating diseases like breast cancer and Alzheimer’s,” Tollefsbol says.

http://www.nature.com/onc/journal/v24/n48/abs/1208874a.html

Oncogene (2005) 24, 7180–7189. doi:10.1038/sj.onc.1208874; published online 11 July 2005

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

http://www.clearviewcancer.com/index.php/newswire/details/542  Clearview Cancer Institute  

Gene maps to transform scientists' work on cancer  

The studies by international scientists and Britain's Wellcome Trust Sanger Institute are the first comprehensive descriptions of tumour cell mutations and lay bare all the genetic changes behind melanoma skin cancer and lung cancer.

AND FINALLY, IODINE DO INDEED CURE SKIN CANCER AS ADVOCATED BY DR. SIMONCINI, so keep your hopes intact, keep an open mind and do your own research. I have given you just a little bit of what is available out there without really getting into what is known as "Alternative Treatments" or "Natural Treatments".

Meanwhile read this blog, one just like yours here, written by those who has been there helping those who just ventured into the skin cancer world and see how they CURED their cancer for good:

http://www.topicalinfo.org/forum/topic.asp?TOPIC_ID=409

I am pasting just a small part of the blog below.. Click the link and read the whole thing and see for yourself. Remember the mind, like a parachute functions only when open!

As I said on the start, when it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire at the same time.

With my best to you all,

Dennis (malenomabegone)

I am moved that you are all concern about my well being and me treatment myself as opposed to quickly surgically removing it. I understand that in your opinion quickly surgically excising it is the best option and I respect that. I am taken by your caring and your support for each other. I joined and posted hoping to let you all know that there is another way, not necessarily as an alternative but as an additional to the traditional.

One replied "I have just read thru the links you posted.  I find that quack-science.  You need more than iodine to cure cancer.  It is insulting to people fighting the cancer fight to declare that "cancer is curable" in a blanket statement like that, and if they are not using your bogus methods then they will lose their fight." 

I would like to address this reply and kind of thinking. What I have presented is not "quack-science" just because "main stream medicine" and yourself do not believe in it's cancer curing ability.  The last thing I want is to be "insulting to people fighting the cancer fight".  However cancer IS curable. (See below.) There are numerous ways to fight cancer and nowhere in my previous post did I ever said that "if they are not using your [my] bogus methods then they will lose their fight" When it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire. I am sorry I made you so angry.

My treatment is based on what is advocated by Dr. Simoncini and Dr. Sircus with additions using what other resources I have at my disposal. It works because sodium bicarbonate is a natural substance produced by the body, the maple syrup (sugar) is for the cancer cells as a Trojan Horse to get the sodium bicarbonate into the cancer cells and the iodine is a topical attack from the surface in. Without sodium bicarbonate you will die. It is used in emergency rooms, resuscitations, cases of acidosis, as well as with chemo therapy so they do not poison the whole patient. Not enough bicarbonate leads to diseases and illnesses ultimately to cancer. Remember that the mind, like a parachute functions only when opened.

You can read them here:

Dr. Simoncini:  http://www.curenaturalicancro.com/index.php

http://www.youtube.com/watch?v=npgyZMaewuE&feature  

Sodium bicarbonate, a natural way to treat the cancer

http://www.imva.info/news/sodium-bicarbonate-baking-soda-cancer-treatment.html

and

http://publications.imva.info/index.php/e-books/sodium-bicarbonate-rich-man-s-poor-man-s-cancer-treatment-e-book.html

I joined this blog to learn from you all with an open mind as well as I hope to contribute back by posting additional modalities of treatment SUCH THAT THE CANCER DOES NOT COME BACK. One just posted that after years of having his/her melanoma removed that a new one came up RIGHT WHERE THE ORIGINAL WAS. What a shame that this has to happen. 

I will first supply some of the information I have on melanoma (in no particular order) and end with how (skin) cancer can be beaten. I apologize that it is going to be long and I hope that for those with an open mind  and want to know as much as possible so you can make a truly informed decision that they find at least some of the following research beneficial. Most are on melanoma while others are to show that cancer CAN indeed be beaten so as not to give up hope. Still others are on what influences the development or prevention of cancer that you yourself can take a proactive role for your own health. For those who do not have the time you may wish to just scan the web sites above of Dr. Simoncini and Dr. Sircus or scroll to the bottom to see the effective treatment of Dr. Simoncini put into practice (and YES) curing skin cancer. Cancer CAN be beaten. It happens everyday.

http://informahealthcare.com/doi/abs/10.1080/13590840802305423

Pharmacokinetics of oral vitamin C

Journal of Nutritional and Environmental Medicine

2008, Vol. 17, No. 3 , Pages 169-177

To determine whether plasma levels above 280 µm L⁻¹, which have selectively killed cancer, bacteria or viruses (in laboratory experiments), can be achieved using oral doses of vitamin C.these information beneficial, which is my purpose in joining this blog, to contribute and to learn in return.

http://oncologystat.com/news/Multiple_Melanomas_in_the_Same_Patient_a_Real_Phenomenon_US.html  Multiple Melanomas in the Same Patient a Real Phenomenon

The chances of a patient's developing multiple primary melanomas over a lifetime is a real phenomenon, with an incidence ranging from 2% to 8% among patients who have had a first melanoma, or an average of about 5%.

Of patients who develop additional melanomas, about 80% develop one in addition to the original, 15% develop two, and the remainder develop three or more. "In my practice I have about four people I follow who have had five or six primary melanomas," said Dr. Burrows, who has practiced dermatology for nearly 40 years and is currently with the division of dermatology at Scripps Clinic Rancho Bernardo in San Diego.

http://oncologystat.com/journals/review_articles/YCTRV/Methods_of_detection_of_circulating_melanoma_cells_A_comparative_overview.html

Methods of detection of circulating melanoma cells: A comparative overview

Cancer Treat Rev. 2011 Jun;37(4):284-290, Andrianos Nezos, Pavlos Msaouel, Nikolaos Pissimissis, Peter Lembessis, Antigone Sourla, Athanasios Armakolas, Helen Gogas, Alexandros J. Stratigos, Andreas D. Katsambas, Michael Koutsilieris

Abstract

Disease dissemination is the major cause of melanoma-related death. A crucial step in the metastatic process is the intravascular invasion and circulation of melanoma cells in the bloodstream with subsequent development of distant micrometastases that is initially clinically undetectable and will eventually progress into clinically apparent metastasis. Therefore, the use of molecular methods to detect circulating melanoma cells may be of value in risk stratification and clinical management of such patients. Herein, we review the currently applied techniques for the detection, isolation, enrichment and further characterization of circulating melanoma cells from peripheral blood samples in melanoma patients. Furthermore, we provide a brief overview of the various molecular markers currently being evaluated as prognostic indicators of melanoma progression.

http://oncologystat.com/journals/review_articles/AEP/Vitamin_D_and_Melanoma.html

Vitamin D and Melanoma

Ann Epidemiol. 2009 Jul;19(7):455-461, Kathleen M. Egan

Abstract

Purpose

Ultraviolet light from sunlight and other sources is the major environmental risk factor for melanoma of the skin. Humans also derive most of their vitamin D from exposure to sunlight. This article reviews current evidence that vitamin D might play a preventive role in the development of melanoma or affect tumor aggressiveness or melanoma patient outcomes.

Methods

Literature review.

Results

The vitamin D receptor has been identified in normal melanocytes as well as melanoma cell lines and primary tissue. A few studies have demonstrated relationships of functional polymorphisms in the vitamin D receptor with melanoma risk or tumor aggressiveness. Identifying an independent influence of vitamin D on melanoma risk is hampered by overwhelming confounding by the carcinogenic influence of ultraviolet radiation on skin melanocytes. Nonetheless an inverse association was suggested in a few studies with greater consumption of dairy foods or other dietary sources. Several lines of evidence are consistent with a potential influence for vitamin D on site-specific aggressiveness of skin melanomas, therapeutic response or patient survival.

Conclusion

Additional research is needed to determine whether vitamin D may have a preventive role in melanoma incidence or a salutary influence on melanoma patient outcome.

http://www.youtube.com/watch?v=KOUR9JSmY3w&feature

Connection with Vitamin D and Cancer

http://articles.mercola.com/sites/articles/archive/2011/11/20/deadly-melanoma-not-due-vitamin-d-deficiency.aspx

The Surprising Cause of Melanoma (And No, it's Not Too Much Sun) Posted By Dr. Mercola | November 20 2011 

http://mercola.fileburst.com/PDF/ExpertInterviewTranscripts/InterviewCaroleBaggerlyVitaminD.pdf

A Special Interview with Carole Baggerly  By Dr. Mercola on Vitamin D and Cancer

http://oncologystat.com/journals/review_articles/SOC/Surgical_Approach_to_Primary_Cutaneous_Melanoma.html

Surgical Approach to Primary Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):39-56, Patrick A. Ott, Russell S. Berman

Abstract

The surgical management of primary cutaneous melanoma, from the diagnostic biopsy through the wide local excision and nodal staging, must be carefully planned, and the biology of the melanoma, microstaging and primary tumor pathologic features of the melanoma, location on the body, patient preferences, and comorbidities must be considered. The treating surgeon must balance preservation of oncologic principles, with optimization of functional and aesthetic outcome. This article reviews the rationale behind the surgical approach in the patient with a primary melanoma.

http://oncologystat.com/journals/ew/YSDIA/Falsepositive_cells_in_sentinel_lymph_nodes.html

False-positive cells in sentinel lymph nodes

Semin Diagn Pathol. 2008 May;25(2):116-119, Jeoffry B. Brennick, Shaofeng Yan

Melanoma sentinel lymph nodes (SLN) are carefully evaluated to maximize sensitivity. Examination includes hematoxylin and eosin (H+E) stained sections at multiple levels through the node, with subsequent immunohistochemical (IHC) stains for melanocytic markers if H+E sections are negative for melanoma. However, not all IHC-positive cells in SLN are metastatic melanoma, as evidenced by the presence of MART-1 positive cells in SLN from breast cancer patients with no history of melanoma (so-called ‘false-positive’ cells). These ‘false-positive cells’ could be nodal nevus, non-melanocytic cells with cross-reacting antigenic determinants, phagocytic cells containing melanocyte antigens, or possibly melanocytes or melanocyte stem cells liberated at the time of biopsy of the cutaneous melanoma. Examination of SLN requires careful correlation of H+E and IHC findings.

http://oncologystat.com/journals/review_articles/SOC/Staging_and_Prognosis_of_Cutaneous_Melanoma.html

Staging and Prognosis of Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):1-17, Paxton V. Dickson, Jeffrey E. Gershenwald

Abstract

Staging of cutaneous melanoma continues to evolve through identification and rigorous analysis of potential prognostic factors. In 1998, the American Joint Committee on Cancer (AJCC) Melanoma Staging Committee developed the AJCC melanoma staging database, an international integrated compilation of prospectively accumulated melanoma outcome data from several centers and clinical trial cooperative groups. Analysis of this database resulted in major revisions to the TNM staging system reflected in the sixth edition of the AJCC Cancer Staging Manual published in 2002. More recently, the committee's analysis of an updated melanoma staging database, including prospective data on more than 50,000 patients, led to staging revisions adopted in the seventh edition of the AJCC Cancer Staging Manual published in 2009. This article highlights these revisions, reviews relevant prognostic factors and their impact on staging, and discusses emerging tools that will likely affect future staging systems and clinical practice.

http://oncologystat.com/journals/review_articles/SOC/EvidenceBased_Followup_for_the_Patient_with_Melanoma.html

Evidence-Based Follow-up for the Patient with Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):181-200, Ryan C. Fields, Daniel G. Coit

Abstract

This article reviews the best evidence available to guide the follow-up of patients with melanoma, focusing on incidence of, and detection of, melanoma recurrence, frequency of follow-up visits, yield of, laboratory and radiographic tests, outcomes of patients with recurrent melanoma based on method of detection, detection of secondary melanomas, and stage-specific follow-up.

http://www.surgonc.theclinics.com/article/S1055-3207(10)00091-8/ppt

Immunotherapy of Melanoma: An Update

·       Jade Homsi, MD, Joshua C. Grimm, BA, Patrick Hwu, MD

     The incidence of melanoma has been increasing worldwide. A relationship between melanoma and the immune system was established years ago. Modulating the immune system in the management of different stages of melanoma has been the focus of numerous large randomized trials worldwide. This article reviews the current status of immunotherapy for melanoma, with a focus on the recent promising results from using vaccines, cytotoxic T-lymphocyte antigen-4 (CTLA-4) antibodies, and adoptive cell therapy.

http://www.ncbi.nlm.nih.gov/pubmed/18022553

Surg Oncol Clin N Am. 2007 Oct;16(4):945-73, xi.

Current immunotherapeutic strategies in malignant melanoma.

Agostino NM, Ali A, Nair SG, Mosca PJ.

Source

Department of Internal Medicine, Lehigh Valley Hospital and Health Network, 1240 South Cedar Crest Boulevard, Allentown, PA 18103, USA.

Abstract

The basis of immunotherapy for melanoma is the existence of melanoma-associated antigens that can be targeted by the immune system. Identification of many of these antigens has enabled investigators to develop a wide array of immunotherapy strategies for the treatment of melanoma. Although several of these strategies have been shown to induce antitumor immune responses in some patients, robust clinical responses have been observed less frequently. With exciting recent advancements in this field, however, there is promise of generating potent immunologic responses and translating them more consistently into durable clinical responses. This article reviews several current approaches to immunotherapy for melanoma and describes the key role that surgeons play in advancing this area of oncology.

http://www.oncologystat.com/journals/journal_scans/Ulceration_and_Stage_Are_Predictive_of_Interferon_Efficacy_In_Melanoma_Results_of_the_Phase_III_Adjuvant_Trials_EORTC_18952_and_EORTC_18991.html 

Ulceration and Stage Are Predictive of Interferon Efficacy In Melanoma: Results of the Phase III Adjuvant Trials EORTC 18952 and EORTC 18991

Breast. 2011 Oct 1;20(3), AMM Eggermont, S Suciu, A Testori, A Spatz, et al

TAKE-HOME MESSAGE

This combined analysis of two large prospective trials of adjuvant interferon for treatment of patients with resected melanoma demonstrated that tumor stage and ulceration predict for immunotherapy benefit.

Abstract

Summary: Adjuvant interferon has modest activity in melanoma patients at high risk for relapse. Patient selection is important; stage and ulceration of the primary tumour are key prognostic factors.

Methods: In this post hoc meta-analysis of European Organisation for Research and Treatment of Cancer (EORTC) trials 18952 (intermediate doses of interferon α-2b [IFN] versus observation in stage IIb-III patients) and 18991 (pegylated [PEG]-IFN versus observation in stage III patients), the predictive value of ulceration on the efficacy of IFN/PEG-IFN with regard to relapse-free survival (RFS), distant metastasis-free survival (DMFS), and overall survival (OS) was assessed in the overall population and in subgroups stratified by stage (IIb and III-N1 [microscopic nodal disease] and III-N2 [macroscopic nodal disease]).

Findings: In the overall population, the comparison of IFN/PEG-IFN versus observation for RFS, DMFS and OS yielded estimated hazard ratios (HR) of 0.85 (p=0.004), 0.89 (p=0.04) and 0.94 (p=0.36), respectively. The impact of treatment was greater in the ulceration group (n=849) compared with the non-ulceration group (n=1336) for RFS (test for interaction: p=0.02), DMFS (p<0.001) and OS (p<0.001). The greatest risk reductions were observed in patients with ulceration and stage IIb/III-N1, with estimated HR for RFS, DMFS, and OS of 0.69 (p=0.003), 0.59 (p<0.0001) and 0.58 (p<0.0001), respectively. The efficacy of IFN/PEG-IFN was lower in stage III-N2 patients with ulceration and uniformly absent in patients without ulceration. There was consistency between the data of both trials.

Interpretation: This meta-analysis of the EORTC 18952 and 18991 trials indicated that both tumour stage and ulceration were predictive factors for the efficacy of adjuvant IFN/PEG-IFN therapy.

http://oncologystat.com/journals/review_articles/archive/Metastatic_Melanoma_An_AJCC_Review.html

or  

http://www.communityoncology.net/co/journal/articles/0508441.pdf

Metastatic Melanoma: An AJCC Review

Community Oncology. 2008 Aug 1;5(8):441-445, SS Agarwala

Abstract

Outside clinical trials, current therapeutic options for patients with metastatic melanoma appear to be of limited benefit. Combination chemotherapy has not been shown to improve outcomes over single-agent chemotherapy, and dacarbazine, which is still the only agent approved by the US Food and Drug Administration for this disease, has produced low response rates and little meaningful improvement in survival. However, with the development and testing of several new compounds, both in the area of immunotherapy and targeted therapy, the future for patients with this disease may become brighter.

News Story: Investigational TKI Active Against Advanced Melanoma in Early Trial »

News Story: Tremelimumab Monotherapy Adds No Benefit Over Chemo in Metastatic Melanoma »

Journal Article: Treatment of Metastatic Melanoma With Autologous CD4+ T Cells Against NY-ESO-1 »

Journal Article: Biochemotherapy for the Treatment of Metastatic Malignant Melanoma: A Systematic Review »

Journal Article: Treatments for Metastatic Melanoma: Synthesis of Evidence From Randomized Trials »

Journal Article: Chemotherapy Compared With Biochemotherapy for the Treatment of Metastatic Melanoma: A Meta-analysis of 18 Trials Involving 2,621 Patients »

http://oncologystat.com/journals/review_articles/HOC/Progress_in_Melanoma_Histopathology_and_Diagnosis.html

Progress in Melanoma Histopathology and Diagnosis

Hematol Oncol Clin North Am. 2009 Jun;23(3):467-480, Adriano Piris, Martin C. Mihm

Abstract

The past 15 years have seen rapid advances in both our understanding of hereditary melanoma genetics and the technologies that enable scientists to make discoveries. Despite great efforts by many groups worldwide, other high-risk melanoma loci besides CDKN2A still remain elusive. A panel of polymorphisms that appears to confer low-to-moderate risk for melanoma has been assembled through functional and genome-wide association studies. The goal of personalized melanoma risk prediction is within our reach, although true clinical use has yet to be established.

http://oncologystat.com/news/Melanoma_Field_Cells_May_Explain_Local_Tumor_Recurrence_US.html  Melanoma Field Cells May Explain Local Tumor Recurrence

Elsevier Global Medical News. 2009 Mar 2, B Jancin  MAUI, HAWAII (EGMN) – The recent discovery of an entity called melanoma field cells that are often present in seemingly normal skin surrounding primary melanomas could ultimately force an overhaul of standard recommended excision margins.

These melanoma field cells are morphologically normal junctional melanocytes and thus cannot be identified using histopathologic criteria. Yet they are genetically melanoma as demonstrated using comparative genomic hybridization and fluorescent in situ hybridization, Dr. Maxwell A. Fung explained at the annual Hawaii Dermatology Seminar sponsored by the Skin Disease Education Foundation.

http://ebm.rsmjournals.com/content/234/8/825.full.pdf+html?sid=658bdab7-e25a-4654-bb4c-ac0d3900cbda

Experimental Biology and Medicine

Molecular Targets of Nutraceuticals Derived from Dietary Spices: Potential Role in Suppression of Inflammation and Tumorigenesis

Overall our review suggests “adding spice to your life” may serve as a healthy and delicious way to ward off cancer and other chronic diseases.

http://journals.lww.com/melanomaresearch/Abstract/2007/10000/Curcumin_downregulates_the_constitutive_activity.2.aspx

Melanoma Research:

October 2007 – Volume 17 – Issue 5 – pp 274-283

doi: 10.1097/CMR.0b013e3282ed3d0e

Original Articles

Curcumin downregulates the constitutive activity of NF-[kappa]B and induces apoptosis in novel mouse melanoma cells

Abstract

Melanoma, the most deadly form of skin cancer, is very aggressive and resistant to present therapies. The transcription factor nuclear factor-kappa B (NF-κB) has been reported to be constitutively active in many types of cancer. Constitutively active NF-κB seen in melanoma likely plays a central role in cell survival and growth. We have established and characterized novel cell lines from our murine melanoma model. Here we report the constitutive activity of NF-κB in these melanoma-derived cells, as shown by electrophoretic mobility shift assay and reporter assays. We hypothesized that agents that inhibit NF-κB may also inhibit cell proliferation and may induce apoptosis in such melanoma cells. Curcumin has been shown to inhibit NF-κB activity in several cell types. In our system, curcumin selectively inhibited growth of melanoma cells, but not normal melanocytes. Curcumin induced melanoma cells to undergo apoptosis, as shown by caspase-3 activation, inversion of membrane phosphatidyl serine, and increases in cells in the sub-G₁ phase. A curcumin dose-dependent inhibition of NF-κB-driven reporter activity correlated with decreased levels of phospho-IκBα, and decreased expression of NF-κB-target genes COX-2 and cyclin D1. This study demonstrates that the use of cells from our model system can facilitate studies of signaling pathways in melanoma. We furthermore conclude that curcumin, a natural and safe compound, inhibits NF-κB activity and the expression of its downstream target genes, and also selectively induces apoptosis of melanoma cells but not normal melanocytes. These encouraging in-vitro results support further investigation of curcumin for treatment of melanoma in vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12680238

Anticancer Res. 2003 Jan-Feb;23(1A):363-98.

Anticancer potential of curcumin: preclinical and clinical studies.

Aggarwal BB, Kumar A, Bharti AC.

Cytokine Research Section, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX, USA. [email protected]

Abstract

Curcumin (diferuloylmethane) is a polyphenol derived from the plant Curcuma longa, commonly called turmeric. Extensive research over the last 50 years has indicated this polyphenol can both prevent and treat cancer. The anticancer potential of curcumin stems from its ability to suppress proliferation of a wide variety of tumor cells, down-regulate transcription factors NF-kappa B, AP-1 and Egr-1; down-regulate the expression of COX2, LOX, NOS, MMP-9, uPA, TNF, chemokines, cell surface adhesion molecules and cyclin D1; down-regulate growth factor receptors (such as EGFR and HER2); and inhibit the activity of c-Jun N-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases. In several systems, curcumin has been described as a potent antioxidant and anti-inflammatory agent. Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis. Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day. All of these studies suggest that curcumin has enormous potential in the prevention and therapy of cancer. The current review describes in detail the data supporting these studies.

http://www.experts.scival.com/wayne/pubDetail.asp?t=pm&id=15252141&amp;

Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation.

http://ur.rutgers.edu/medrel/viewArticle.html?ArticleID=49

 Rutgers, The State University of New Jersey: Curry and Cauliflower Could Halt Prostate Cancer

http://www.jcrows.com/curryfightsprostatecancer.html  

Curry fights prostate cancer, study finds

http://mss3.libraries.rutgers.edu/dlr/showfed.php?pid=rutgers-lib:25088  

Prostate cancer chemoprevention by dietary phytochemicals: 

Chemoprevention entails the use of preferably dietary agents to block or suppress the various stages of prostate carcinogenesis. Flavonoids, the essential components of fruits and vegetables can modulate transcription factor AP-1 and its upstream signaling cascades mainly ERK-MAPK and JNK-MAPK in human androgen insensitive prostate cancer (PC3) cells. Soy isoflavone concentrate can upregulate the expression of several phase II detoxifying and antioxidant genes in an NF-E2-related factor 2 (Nrf2) dependent manner. In addition to detoxifying genes, soy isoflavone concentrate can also modulate the expression of genes such as LATS2, GREB1, calpain and many more in an Nrf2 dependent manner. 

In one such transgenic model, curcumin or PEITC suppressed high grade PIN levels. However a combination of low doses of these agents worked remarkably well in suppressing tumors all together.

http://www.newswise.com/articles/view/573327/

Genetic Evidence That Antioxidants Can Help Treat Cancer  

“Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth,” said lead researcher Michael P. Lisanti, M.D., Ph.D., professor of cancer biology at Jefferson Medical College of Thomas Jefferson University and member of the Kimmel Cancer Center at Jefferson. “This means we need to make anti-cancer drugs that specially target this type of oxidative stress. And there are already antioxidant drugs out there on the market as dietary supplements, like N-acetyl cysteine.” 

The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.

“Antioxidants have been associated with cancer reducing effects—beta carotene, for example—but the mechanisms, the genetic evidence, has been lacking,” Dr. Lisanti said. “This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth.”

 These findings were originally published in the online February 15 issue of Cancer Biology & Therapy.

http://cancerres.aacrjournals.org/content/71/13/4484

A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.

http://www.newswise.com/articles/view/574151/?sc=mwhn

Biologists Show How Veggies Work in Cancer-Fighting Diet

Released: 3/7/2011 3:00 PM EST 

Source: University of Alabama at Birmingham

Newswise — BIRMINGHAM, Ala. – Mothers around the world now collectively can say, “I told you so.”

Your vegetables are good for you, says a research review published by scientists from the University of Alabama at Birmingham in the journal Clinical Epigenetics.

In particular, vegetables such as broccoli and cabbage are filled with compounds that could help reverse or prevent cancers and other aging-related diseases as part of the “epigenetics diet,” a new lifestyle concept coined after the article’s publication.

“Your mother always told you to eat your vegetables, and she was right,” says co-author Trygve Tollefsbol, Ph.D., D.O., a biology professor in the UAB College of Arts and Sciences. “But now we better understand why she was right — compounds in many of these foods suppress gene aberrations that over time cause fatal diseases.”

Epigenetics is the study of the changes in human gene expressions with time, changes that can cause cancer and Alzheimer’s, among other diseases. In recent years, epigenetics research worldwide, including numerous studies conducted at UAB, have identified specific food compounds that inhibit negative epigenetic effects.

Those foods include soybeans, cauliflower, broccoli and cabbage. Green tea, fava beans, kale, grapes and the spice turmeric round out the diet.

“The epigenetics diet can be adopted easily, because the concentrations of the compounds needed for a positive effect are readily achievable,” says lead author Syed Meeran, Ph.D., a research assistant professor in Tollefsbol’s UAB Department of Biology laboratory.

For example, Meeran says sipping tea compounds called polyphenols in daily amounts that are equivalent to approximately three cups of green tea has been shown to reverse breast cancer in laboratory mice by suppressing the gene that triggers the disease. Similarly, a daily cup of broccoli sprouts, which has sulforaphane as an active compound, has been shown to reduce the risk of developing many cancers.

“Our review article has drawn everything together from global studies, and the common theme is that compounds in the epigenetics diet foods can, at the very least, help us lead healthier lives and help our bodies prevent potentially debilitating diseases like breast cancer and Alzheimer’s,” Tollefsbol says.

http://www.nature.com/onc/journal/v24/n48/abs/1208874a.html

Oncogene (2005) 24, 7180–7189. doi:10.1038/sj.onc.1208874; published online 11 July 2005

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

http://www.clearviewcancer.com/index.php/newswire/details/542  Clearview Cancer Institute  

Gene maps to transform scientists' work on cancer  

The studies by international scientists and Britain's Wellcome Trust Sanger Institute are the first comprehensive descriptions of tumour cell mutations and lay bare all the genetic changes behind melanoma skin cancer and lung cancer.

AND FINALLY, IODINE DO INDEED CURE SKIN CANCER AS ADVOCATED BY DR. SIMONCINI, so keep your hopes intact, keep an open mind and do your own research. I have given you just a little bit of what is available out there without really getting into what is known as "Alternative Treatments" or "Natural Treatments".

Meanwhile read this blog, one just like yours here, written by those who has been there helping those who just ventured into the skin cancer world and see how they CURED their cancer for good:

http://www.topicalinfo.org/forum/topic.asp?TOPIC_ID=409

I am pasting just a small part of the blog below.. Click the link and read the whole thing and see for yourself. Remember the mind, like a parachute functions only when open!

As I said on the start, when it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire at the same time.

With my best to you all,

Dennis (malenomabegone)

I am moved that you are all concern about my well being and me treatment myself as opposed to quickly surgically removing it. I understand that in your opinion quickly surgically excising it is the best option and I respect that. I am taken by your caring and your support for each other. I joined and posted hoping to let you all know that there is another way, not necessarily as an alternative but as an additional to the traditional.

One replied "I have just read thru the links you posted.  I find that quack-science.  You need more than iodine to cure cancer.  It is insulting to people fighting the cancer fight to declare that "cancer is curable" in a blanket statement like that, and if they are not using your bogus methods then they will lose their fight." 

I would like to address this reply and kind of thinking. What I have presented is not "quack-science" just because "main stream medicine" and yourself do not believe in it's cancer curing ability.  The last thing I want is to be "insulting to people fighting the cancer fight".  However cancer IS curable. (See below.) There are numerous ways to fight cancer and nowhere in my previous post did I ever said that "if they are not using your [my] bogus methods then they will lose their fight" When it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire. I am sorry I made you so angry.

My treatment is based on what is advocated by Dr. Simoncini and Dr. Sircus with additions using what other resources I have at my disposal. It works because sodium bicarbonate is a natural substance produced by the body, the maple syrup (sugar) is for the cancer cells as a Trojan Horse to get the sodium bicarbonate into the cancer cells and the iodine is a topical attack from the surface in. Without sodium bicarbonate you will die. It is used in emergency rooms, resuscitations, cases of acidosis, as well as with chemo therapy so they do not poison the whole patient. Not enough bicarbonate leads to diseases and illnesses ultimately to cancer. Remember that the mind, like a parachute functions only when opened.

You can read them here:

Dr. Simoncini:  http://www.curenaturalicancro.com/index.php

http://www.youtube.com/watch?v=npgyZMaewuE&feature  

Sodium bicarbonate, a natural way to treat the cancer

http://www.imva.info/news/sodium-bicarbonate-baking-soda-cancer-treatment.html

and

http://publications.imva.info/index.php/e-books/sodium-bicarbonate-rich-man-s-poor-man-s-cancer-treatment-e-book.html

I joined this blog to learn from you all with an open mind as well as I hope to contribute back by posting additional modalities of treatment SUCH THAT THE CANCER DOES NOT COME BACK. One just posted that after years of having his/her melanoma removed that a new one came up RIGHT WHERE THE ORIGINAL WAS. What a shame that this has to happen. 

I will first supply some of the information I have on melanoma (in no particular order) and end with how (skin) cancer can be beaten. I apologize that it is going to be long and I hope that for those with an open mind  and want to know as much as possible so you can make a truly informed decision that they find at least some of the following research beneficial. Most are on melanoma while others are to show that cancer CAN indeed be beaten so as not to give up hope. Still others are on what influences the development or prevention of cancer that you yourself can take a proactive role for your own health. For those who do not have the time you may wish to just scan the web sites above of Dr. Simoncini and Dr. Sircus or scroll to the bottom to see the effective treatment of Dr. Simoncini put into practice (and YES) curing skin cancer. Cancer CAN be beaten. It happens everyday.

http://informahealthcare.com/doi/abs/10.1080/13590840802305423

Pharmacokinetics of oral vitamin C

Journal of Nutritional and Environmental Medicine

2008, Vol. 17, No. 3 , Pages 169-177

To determine whether plasma levels above 280 µm L⁻¹, which have selectively killed cancer, bacteria or viruses (in laboratory experiments), can be achieved using oral doses of vitamin C.these information beneficial, which is my purpose in joining this blog, to contribute and to learn in return.

http://oncologystat.com/news/Multiple_Melanomas_in_the_Same_Patient_a_Real_Phenomenon_US.html  Multiple Melanomas in the Same Patient a Real Phenomenon

The chances of a patient's developing multiple primary melanomas over a lifetime is a real phenomenon, with an incidence ranging from 2% to 8% among patients who have had a first melanoma, or an average of about 5%.

Of patients who develop additional melanomas, about 80% develop one in addition to the original, 15% develop two, and the remainder develop three or more. "In my practice I have about four people I follow who have had five or six primary melanomas," said Dr. Burrows, who has practiced dermatology for nearly 40 years and is currently with the division of dermatology at Scripps Clinic Rancho Bernardo in San Diego.

http://oncologystat.com/journals/review_articles/YCTRV/Methods_of_detection_of_circulating_melanoma_cells_A_comparative_overview.html

Methods of detection of circulating melanoma cells: A comparative overview

Cancer Treat Rev. 2011 Jun;37(4):284-290, Andrianos Nezos, Pavlos Msaouel, Nikolaos Pissimissis, Peter Lembessis, Antigone Sourla, Athanasios Armakolas, Helen Gogas, Alexandros J. Stratigos, Andreas D. Katsambas, Michael Koutsilieris

Abstract

Disease dissemination is the major cause of melanoma-related death. A crucial step in the metastatic process is the intravascular invasion and circulation of melanoma cells in the bloodstream with subsequent development of distant micrometastases that is initially clinically undetectable and will eventually progress into clinically apparent metastasis. Therefore, the use of molecular methods to detect circulating melanoma cells may be of value in risk stratification and clinical management of such patients. Herein, we review the currently applied techniques for the detection, isolation, enrichment and further characterization of circulating melanoma cells from peripheral blood samples in melanoma patients. Furthermore, we provide a brief overview of the various molecular markers currently being evaluated as prognostic indicators of melanoma progression.

http://oncologystat.com/journals/review_articles/AEP/Vitamin_D_and_Melanoma.html

Vitamin D and Melanoma

Ann Epidemiol. 2009 Jul;19(7):455-461, Kathleen M. Egan

Abstract

Purpose

Ultraviolet light from sunlight and other sources is the major environmental risk factor for melanoma of the skin. Humans also derive most of their vitamin D from exposure to sunlight. This article reviews current evidence that vitamin D might play a preventive role in the development of melanoma or affect tumor aggressiveness or melanoma patient outcomes.

Methods

Literature review.

Results

The vitamin D receptor has been identified in normal melanocytes as well as melanoma cell lines and primary tissue. A few studies have demonstrated relationships of functional polymorphisms in the vitamin D receptor with melanoma risk or tumor aggressiveness. Identifying an independent influence of vitamin D on melanoma risk is hampered by overwhelming confounding by the carcinogenic influence of ultraviolet radiation on skin melanocytes. Nonetheless an inverse association was suggested in a few studies with greater consumption of dairy foods or other dietary sources. Several lines of evidence are consistent with a potential influence for vitamin D on site-specific aggressiveness of skin melanomas, therapeutic response or patient survival.

Conclusion

Additional research is needed to determine whether vitamin D may have a preventive role in melanoma incidence or a salutary influence on melanoma patient outcome.

http://www.youtube.com/watch?v=KOUR9JSmY3w&feature

Connection with Vitamin D and Cancer

http://articles.mercola.com/sites/articles/archive/2011/11/20/deadly-melanoma-not-due-vitamin-d-deficiency.aspx

The Surprising Cause of Melanoma (And No, it's Not Too Much Sun) Posted By Dr. Mercola | November 20 2011 

http://mercola.fileburst.com/PDF/ExpertInterviewTranscripts/InterviewCaroleBaggerlyVitaminD.pdf

A Special Interview with Carole Baggerly  By Dr. Mercola on Vitamin D and Cancer

http://oncologystat.com/journals/review_articles/SOC/Surgical_Approach_to_Primary_Cutaneous_Melanoma.html

Surgical Approach to Primary Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):39-56, Patrick A. Ott, Russell S. Berman

Abstract

The surgical management of primary cutaneous melanoma, from the diagnostic biopsy through the wide local excision and nodal staging, must be carefully planned, and the biology of the melanoma, microstaging and primary tumor pathologic features of the melanoma, location on the body, patient preferences, and comorbidities must be considered. The treating surgeon must balance preservation of oncologic principles, with optimization of functional and aesthetic outcome. This article reviews the rationale behind the surgical approach in the patient with a primary melanoma.

http://oncologystat.com/journals/ew/YSDIA/Falsepositive_cells_in_sentinel_lymph_nodes.html

False-positive cells in sentinel lymph nodes

Semin Diagn Pathol. 2008 May;25(2):116-119, Jeoffry B. Brennick, Shaofeng Yan

Melanoma sentinel lymph nodes (SLN) are carefully evaluated to maximize sensitivity. Examination includes hematoxylin and eosin (H+E) stained sections at multiple levels through the node, with subsequent immunohistochemical (IHC) stains for melanocytic markers if H+E sections are negative for melanoma. However, not all IHC-positive cells in SLN are metastatic melanoma, as evidenced by the presence of MART-1 positive cells in SLN from breast cancer patients with no history of melanoma (so-called ‘false-positive’ cells). These ‘false-positive cells’ could be nodal nevus, non-melanocytic cells with cross-reacting antigenic determinants, phagocytic cells containing melanocyte antigens, or possibly melanocytes or melanocyte stem cells liberated at the time of biopsy of the cutaneous melanoma. Examination of SLN requires careful correlation of H+E and IHC findings.

http://oncologystat.com/journals/review_articles/SOC/Staging_and_Prognosis_of_Cutaneous_Melanoma.html

Staging and Prognosis of Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):1-17, Paxton V. Dickson, Jeffrey E. Gershenwald

Abstract

Staging of cutaneous melanoma continues to evolve through identification and rigorous analysis of potential prognostic factors. In 1998, the American Joint Committee on Cancer (AJCC) Melanoma Staging Committee developed the AJCC melanoma staging database, an international integrated compilation of prospectively accumulated melanoma outcome data from several centers and clinical trial cooperative groups. Analysis of this database resulted in major revisions to the TNM staging system reflected in the sixth edition of the AJCC Cancer Staging Manual published in 2002. More recently, the committee's analysis of an updated melanoma staging database, including prospective data on more than 50,000 patients, led to staging revisions adopted in the seventh edition of the AJCC Cancer Staging Manual published in 2009. This article highlights these revisions, reviews relevant prognostic factors and their impact on staging, and discusses emerging tools that will likely affect future staging systems and clinical practice.

http://oncologystat.com/journals/review_articles/SOC/EvidenceBased_Followup_for_the_Patient_with_Melanoma.html

Evidence-Based Follow-up for the Patient with Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):181-200, Ryan C. Fields, Daniel G. Coit

Abstract

This article reviews the best evidence available to guide the follow-up of patients with melanoma, focusing on incidence of, and detection of, melanoma recurrence, frequency of follow-up visits, yield of, laboratory and radiographic tests, outcomes of patients with recurrent melanoma based on method of detection, detection of secondary melanomas, and stage-specific follow-up.

http://www.surgonc.theclinics.com/article/S1055-3207(10)00091-8/ppt

Immunotherapy of Melanoma: An Update

·       Jade Homsi, MD, Joshua C. Grimm, BA, Patrick Hwu, MD

     The incidence of melanoma has been increasing worldwide. A relationship between melanoma and the immune system was established years ago. Modulating the immune system in the management of different stages of melanoma has been the focus of numerous large randomized trials worldwide. This article reviews the current status of immunotherapy for melanoma, with a focus on the recent promising results from using vaccines, cytotoxic T-lymphocyte antigen-4 (CTLA-4) antibodies, and adoptive cell therapy.

http://www.ncbi.nlm.nih.gov/pubmed/18022553

Surg Oncol Clin N Am. 2007 Oct;16(4):945-73, xi.

Current immunotherapeutic strategies in malignant melanoma.

Agostino NM, Ali A, Nair SG, Mosca PJ.

Source

Department of Internal Medicine, Lehigh Valley Hospital and Health Network, 1240 South Cedar Crest Boulevard, Allentown, PA 18103, USA.

Abstract

The basis of immunotherapy for melanoma is the existence of melanoma-associated antigens that can be targeted by the immune system. Identification of many of these antigens has enabled investigators to develop a wide array of immunotherapy strategies for the treatment of melanoma. Although several of these strategies have been shown to induce antitumor immune responses in some patients, robust clinical responses have been observed less frequently. With exciting recent advancements in this field, however, there is promise of generating potent immunologic responses and translating them more consistently into durable clinical responses. This article reviews several current approaches to immunotherapy for melanoma and describes the key role that surgeons play in advancing this area of oncology.

http://www.oncologystat.com/journals/journal_scans/Ulceration_and_Stage_Are_Predictive_of_Interferon_Efficacy_In_Melanoma_Results_of_the_Phase_III_Adjuvant_Trials_EORTC_18952_and_EORTC_18991.html 

Ulceration and Stage Are Predictive of Interferon Efficacy In Melanoma: Results of the Phase III Adjuvant Trials EORTC 18952 and EORTC 18991

Breast. 2011 Oct 1;20(3), AMM Eggermont, S Suciu, A Testori, A Spatz, et al

TAKE-HOME MESSAGE

This combined analysis of two large prospective trials of adjuvant interferon for treatment of patients with resected melanoma demonstrated that tumor stage and ulceration predict for immunotherapy benefit.

Abstract

Summary: Adjuvant interferon has modest activity in melanoma patients at high risk for relapse. Patient selection is important; stage and ulceration of the primary tumour are key prognostic factors.

Methods: In this post hoc meta-analysis of European Organisation for Research and Treatment of Cancer (EORTC) trials 18952 (intermediate doses of interferon α-2b [IFN] versus observation in stage IIb-III patients) and 18991 (pegylated [PEG]-IFN versus observation in stage III patients), the predictive value of ulceration on the efficacy of IFN/PEG-IFN with regard to relapse-free survival (RFS), distant metastasis-free survival (DMFS), and overall survival (OS) was assessed in the overall population and in subgroups stratified by stage (IIb and III-N1 [microscopic nodal disease] and III-N2 [macroscopic nodal disease]).

Findings: In the overall population, the comparison of IFN/PEG-IFN versus observation for RFS, DMFS and OS yielded estimated hazard ratios (HR) of 0.85 (p=0.004), 0.89 (p=0.04) and 0.94 (p=0.36), respectively. The impact of treatment was greater in the ulceration group (n=849) compared with the non-ulceration group (n=1336) for RFS (test for interaction: p=0.02), DMFS (p<0.001) and OS (p<0.001). The greatest risk reductions were observed in patients with ulceration and stage IIb/III-N1, with estimated HR for RFS, DMFS, and OS of 0.69 (p=0.003), 0.59 (p<0.0001) and 0.58 (p<0.0001), respectively. The efficacy of IFN/PEG-IFN was lower in stage III-N2 patients with ulceration and uniformly absent in patients without ulceration. There was consistency between the data of both trials.

Interpretation: This meta-analysis of the EORTC 18952 and 18991 trials indicated that both tumour stage and ulceration were predictive factors for the efficacy of adjuvant IFN/PEG-IFN therapy.

http://oncologystat.com/journals/review_articles/archive/Metastatic_Melanoma_An_AJCC_Review.html

or  

http://www.communityoncology.net/co/journal/articles/0508441.pdf

Metastatic Melanoma: An AJCC Review

Community Oncology. 2008 Aug 1;5(8):441-445, SS Agarwala

Abstract

Outside clinical trials, current therapeutic options for patients with metastatic melanoma appear to be of limited benefit. Combination chemotherapy has not been shown to improve outcomes over single-agent chemotherapy, and dacarbazine, which is still the only agent approved by the US Food and Drug Administration for this disease, has produced low response rates and little meaningful improvement in survival. However, with the development and testing of several new compounds, both in the area of immunotherapy and targeted therapy, the future for patients with this disease may become brighter.

News Story: Investigational TKI Active Against Advanced Melanoma in Early Trial »

News Story: Tremelimumab Monotherapy Adds No Benefit Over Chemo in Metastatic Melanoma »

Journal Article: Treatment of Metastatic Melanoma With Autologous CD4+ T Cells Against NY-ESO-1 »

Journal Article: Biochemotherapy for the Treatment of Metastatic Malignant Melanoma: A Systematic Review »

Journal Article: Treatments for Metastatic Melanoma: Synthesis of Evidence From Randomized Trials »

Journal Article: Chemotherapy Compared With Biochemotherapy for the Treatment of Metastatic Melanoma: A Meta-analysis of 18 Trials Involving 2,621 Patients »

http://oncologystat.com/journals/review_articles/HOC/Progress_in_Melanoma_Histopathology_and_Diagnosis.html

Progress in Melanoma Histopathology and Diagnosis

Hematol Oncol Clin North Am. 2009 Jun;23(3):467-480, Adriano Piris, Martin C. Mihm

Abstract

The past 15 years have seen rapid advances in both our understanding of hereditary melanoma genetics and the technologies that enable scientists to make discoveries. Despite great efforts by many groups worldwide, other high-risk melanoma loci besides CDKN2A still remain elusive. A panel of polymorphisms that appears to confer low-to-moderate risk for melanoma has been assembled through functional and genome-wide association studies. The goal of personalized melanoma risk prediction is within our reach, although true clinical use has yet to be established.

http://oncologystat.com/news/Melanoma_Field_Cells_May_Explain_Local_Tumor_Recurrence_US.html  Melanoma Field Cells May Explain Local Tumor Recurrence

Elsevier Global Medical News. 2009 Mar 2, B Jancin  MAUI, HAWAII (EGMN) – The recent discovery of an entity called melanoma field cells that are often present in seemingly normal skin surrounding primary melanomas could ultimately force an overhaul of standard recommended excision margins.

These melanoma field cells are morphologically normal junctional melanocytes and thus cannot be identified using histopathologic criteria. Yet they are genetically melanoma as demonstrated using comparative genomic hybridization and fluorescent in situ hybridization, Dr. Maxwell A. Fung explained at the annual Hawaii Dermatology Seminar sponsored by the Skin Disease Education Foundation.

http://ebm.rsmjournals.com/content/234/8/825.full.pdf+html?sid=658bdab7-e25a-4654-bb4c-ac0d3900cbda

Experimental Biology and Medicine

Molecular Targets of Nutraceuticals Derived from Dietary Spices: Potential Role in Suppression of Inflammation and Tumorigenesis

Overall our review suggests “adding spice to your life” may serve as a healthy and delicious way to ward off cancer and other chronic diseases.

http://journals.lww.com/melanomaresearch/Abstract/2007/10000/Curcumin_downregulates_the_constitutive_activity.2.aspx

Melanoma Research:

October 2007 – Volume 17 – Issue 5 – pp 274-283

doi: 10.1097/CMR.0b013e3282ed3d0e

Original Articles

Curcumin downregulates the constitutive activity of NF-[kappa]B and induces apoptosis in novel mouse melanoma cells

Abstract

Melanoma, the most deadly form of skin cancer, is very aggressive and resistant to present therapies. The transcription factor nuclear factor-kappa B (NF-κB) has been reported to be constitutively active in many types of cancer. Constitutively active NF-κB seen in melanoma likely plays a central role in cell survival and growth. We have established and characterized novel cell lines from our murine melanoma model. Here we report the constitutive activity of NF-κB in these melanoma-derived cells, as shown by electrophoretic mobility shift assay and reporter assays. We hypothesized that agents that inhibit NF-κB may also inhibit cell proliferation and may induce apoptosis in such melanoma cells. Curcumin has been shown to inhibit NF-κB activity in several cell types. In our system, curcumin selectively inhibited growth of melanoma cells, but not normal melanocytes. Curcumin induced melanoma cells to undergo apoptosis, as shown by caspase-3 activation, inversion of membrane phosphatidyl serine, and increases in cells in the sub-G₁ phase. A curcumin dose-dependent inhibition of NF-κB-driven reporter activity correlated with decreased levels of phospho-IκBα, and decreased expression of NF-κB-target genes COX-2 and cyclin D1. This study demonstrates that the use of cells from our model system can facilitate studies of signaling pathways in melanoma. We furthermore conclude that curcumin, a natural and safe compound, inhibits NF-κB activity and the expression of its downstream target genes, and also selectively induces apoptosis of melanoma cells but not normal melanocytes. These encouraging in-vitro results support further investigation of curcumin for treatment of melanoma in vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12680238

Anticancer Res. 2003 Jan-Feb;23(1A):363-98.

Anticancer potential of curcumin: preclinical and clinical studies.

Aggarwal BB, Kumar A, Bharti AC.

Cytokine Research Section, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX, USA. [email protected]

Abstract

Curcumin (diferuloylmethane) is a polyphenol derived from the plant Curcuma longa, commonly called turmeric. Extensive research over the last 50 years has indicated this polyphenol can both prevent and treat cancer. The anticancer potential of curcumin stems from its ability to suppress proliferation of a wide variety of tumor cells, down-regulate transcription factors NF-kappa B, AP-1 and Egr-1; down-regulate the expression of COX2, LOX, NOS, MMP-9, uPA, TNF, chemokines, cell surface adhesion molecules and cyclin D1; down-regulate growth factor receptors (such as EGFR and HER2); and inhibit the activity of c-Jun N-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases. In several systems, curcumin has been described as a potent antioxidant and anti-inflammatory agent. Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis. Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day. All of these studies suggest that curcumin has enormous potential in the prevention and therapy of cancer. The current review describes in detail the data supporting these studies.

http://www.experts.scival.com/wayne/pubDetail.asp?t=pm&id=15252141&amp;

Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation.

http://ur.rutgers.edu/medrel/viewArticle.html?ArticleID=49

 Rutgers, The State University of New Jersey: Curry and Cauliflower Could Halt Prostate Cancer

http://www.jcrows.com/curryfightsprostatecancer.html  

Curry fights prostate cancer, study finds

http://mss3.libraries.rutgers.edu/dlr/showfed.php?pid=rutgers-lib:25088  

Prostate cancer chemoprevention by dietary phytochemicals: 

Chemoprevention entails the use of preferably dietary agents to block or suppress the various stages of prostate carcinogenesis. Flavonoids, the essential components of fruits and vegetables can modulate transcription factor AP-1 and its upstream signaling cascades mainly ERK-MAPK and JNK-MAPK in human androgen insensitive prostate cancer (PC3) cells. Soy isoflavone concentrate can upregulate the expression of several phase II detoxifying and antioxidant genes in an NF-E2-related factor 2 (Nrf2) dependent manner. In addition to detoxifying genes, soy isoflavone concentrate can also modulate the expression of genes such as LATS2, GREB1, calpain and many more in an Nrf2 dependent manner. 

In one such transgenic model, curcumin or PEITC suppressed high grade PIN levels. However a combination of low doses of these agents worked remarkably well in suppressing tumors all together.

http://www.newswise.com/articles/view/573327/

Genetic Evidence That Antioxidants Can Help Treat Cancer  

“Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth,” said lead researcher Michael P. Lisanti, M.D., Ph.D., professor of cancer biology at Jefferson Medical College of Thomas Jefferson University and member of the Kimmel Cancer Center at Jefferson. “This means we need to make anti-cancer drugs that specially target this type of oxidative stress. And there are already antioxidant drugs out there on the market as dietary supplements, like N-acetyl cysteine.” 

The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.

“Antioxidants have been associated with cancer reducing effects—beta carotene, for example—but the mechanisms, the genetic evidence, has been lacking,” Dr. Lisanti said. “This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth.”

 These findings were originally published in the online February 15 issue of Cancer Biology & Therapy.

http://cancerres.aacrjournals.org/content/71/13/4484

A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.

http://www.newswise.com/articles/view/574151/?sc=mwhn

Biologists Show How Veggies Work in Cancer-Fighting Diet

Released: 3/7/2011 3:00 PM EST 

Source: University of Alabama at Birmingham

Newswise — BIRMINGHAM, Ala. – Mothers around the world now collectively can say, “I told you so.”

Your vegetables are good for you, says a research review published by scientists from the University of Alabama at Birmingham in the journal Clinical Epigenetics.

In particular, vegetables such as broccoli and cabbage are filled with compounds that could help reverse or prevent cancers and other aging-related diseases as part of the “epigenetics diet,” a new lifestyle concept coined after the article’s publication.

“Your mother always told you to eat your vegetables, and she was right,” says co-author Trygve Tollefsbol, Ph.D., D.O., a biology professor in the UAB College of Arts and Sciences. “But now we better understand why she was right — compounds in many of these foods suppress gene aberrations that over time cause fatal diseases.”

Epigenetics is the study of the changes in human gene expressions with time, changes that can cause cancer and Alzheimer’s, among other diseases. In recent years, epigenetics research worldwide, including numerous studies conducted at UAB, have identified specific food compounds that inhibit negative epigenetic effects.

Those foods include soybeans, cauliflower, broccoli and cabbage. Green tea, fava beans, kale, grapes and the spice turmeric round out the diet.

“The epigenetics diet can be adopted easily, because the concentrations of the compounds needed for a positive effect are readily achievable,” says lead author Syed Meeran, Ph.D., a research assistant professor in Tollefsbol’s UAB Department of Biology laboratory.

For example, Meeran says sipping tea compounds called polyphenols in daily amounts that are equivalent to approximately three cups of green tea has been shown to reverse breast cancer in laboratory mice by suppressing the gene that triggers the disease. Similarly, a daily cup of broccoli sprouts, which has sulforaphane as an active compound, has been shown to reduce the risk of developing many cancers.

“Our review article has drawn everything together from global studies, and the common theme is that compounds in the epigenetics diet foods can, at the very least, help us lead healthier lives and help our bodies prevent potentially debilitating diseases like breast cancer and Alzheimer’s,” Tollefsbol says.

http://www.nature.com/onc/journal/v24/n48/abs/1208874a.html

Oncogene (2005) 24, 7180–7189. doi:10.1038/sj.onc.1208874; published online 11 July 2005

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

http://www.clearviewcancer.com/index.php/newswire/details/542  Clearview Cancer Institute  

Gene maps to transform scientists' work on cancer  

The studies by international scientists and Britain's Wellcome Trust Sanger Institute are the first comprehensive descriptions of tumour cell mutations and lay bare all the genetic changes behind melanoma skin cancer and lung cancer.

AND FINALLY, IODINE DO INDEED CURE SKIN CANCER AS ADVOCATED BY DR. SIMONCINI, so keep your hopes intact, keep an open mind and do your own research. I have given you just a little bit of what is available out there without really getting into what is known as "Alternative Treatments" or "Natural Treatments".

Meanwhile read this blog, one just like yours here, written by those who has been there helping those who just ventured into the skin cancer world and see how they CURED their cancer for good:

http://www.topicalinfo.org/forum/topic.asp?TOPIC_ID=409

I am pasting just a small part of the blog below.. Click the link and read the whole thing and see for yourself. Remember the mind, like a parachute functions only when open!

As I said on the start, when it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire at the same time.

With my best to you all,

Dennis (malenomabegone)

I am moved that you are all concern about my well being and me treatment myself as opposed to quickly surgically removing it. I understand that in your opinion quickly surgically excising it is the best option and I respect that. I am taken by your caring and your support for each other. I joined and posted hoping to let you all know that there is another way, not necessarily as an alternative but as an additional to the traditional.

One replied "I have just read thru the links you posted.  I find that quack-science.  You need more than iodine to cure cancer.  It is insulting to people fighting the cancer fight to declare that "cancer is curable" in a blanket statement like that, and if they are not using your bogus methods then they will lose their fight." 

I would like to address this reply and kind of thinking. What I have presented is not "quack-science" just because "main stream medicine" and yourself do not believe in it's cancer curing ability.  The last thing I want is to be "insulting to people fighting the cancer fight".  However cancer IS curable. (See below.) There are numerous ways to fight cancer and nowhere in my previous post did I ever said that "if they are not using your [my] bogus methods then they will lose their fight" When it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire. I am sorry I made you so angry.

My treatment is based on what is advocated by Dr. Simoncini and Dr. Sircus with additions using what other resources I have at my disposal. It works because sodium bicarbonate is a natural substance produced by the body, the maple syrup (sugar) is for the cancer cells as a Trojan Horse to get the sodium bicarbonate into the cancer cells and the iodine is a topical attack from the surface in. Without sodium bicarbonate you will die. It is used in emergency rooms, resuscitations, cases of acidosis, as well as with chemo therapy so they do not poison the whole patient. Not enough bicarbonate leads to diseases and illnesses ultimately to cancer. Remember that the mind, like a parachute functions only when opened.

You can read them here:

Dr. Simoncini:  http://www.curenaturalicancro.com/index.php

http://www.youtube.com/watch?v=npgyZMaewuE&feature  

Sodium bicarbonate, a natural way to treat the cancer

http://www.imva.info/news/sodium-bicarbonate-baking-soda-cancer-treatment.html

and

http://publications.imva.info/index.php/e-books/sodium-bicarbonate-rich-man-s-poor-man-s-cancer-treatment-e-book.html

I joined this blog to learn from you all with an open mind as well as I hope to contribute back by posting additional modalities of treatment SUCH THAT THE CANCER DOES NOT COME BACK. One just posted that after years of having his/her melanoma removed that a new one came up RIGHT WHERE THE ORIGINAL WAS. What a shame that this has to happen. 

I will first supply some of the information I have on melanoma (in no particular order) and end with how (skin) cancer can be beaten. I apologize that it is going to be long and I hope that for those with an open mind  and want to know as much as possible so you can make a truly informed decision that they find at least some of the following research beneficial. Most are on melanoma while others are to show that cancer CAN indeed be beaten so as not to give up hope. Still others are on what influences the development or prevention of cancer that you yourself can take a proactive role for your own health. For those who do not have the time you may wish to just scan the web sites above of Dr. Simoncini and Dr. Sircus or scroll to the bottom to see the effective treatment of Dr. Simoncini put into practice (and YES) curing skin cancer. Cancer CAN be beaten. It happens everyday.

http://informahealthcare.com/doi/abs/10.1080/13590840802305423

Pharmacokinetics of oral vitamin C

Journal of Nutritional and Environmental Medicine

2008, Vol. 17, No. 3 , Pages 169-177

To determine whether plasma levels above 280 µm L⁻¹, which have selectively killed cancer, bacteria or viruses (in laboratory experiments), can be achieved using oral doses of vitamin C.these information beneficial, which is my purpose in joining this blog, to contribute and to learn in return.

http://oncologystat.com/news/Multiple_Melanomas_in_the_Same_Patient_a_Real_Phenomenon_US.html  Multiple Melanomas in the Same Patient a Real Phenomenon

The chances of a patient's developing multiple primary melanomas over a lifetime is a real phenomenon, with an incidence ranging from 2% to 8% among patients who have had a first melanoma, or an average of about 5%.

Of patients who develop additional melanomas, about 80% develop one in addition to the original, 15% develop two, and the remainder develop three or more. "In my practice I have about four people I follow who have had five or six primary melanomas," said Dr. Burrows, who has practiced dermatology for nearly 40 years and is currently with the division of dermatology at Scripps Clinic Rancho Bernardo in San Diego.

http://oncologystat.com/journals/review_articles/YCTRV/Methods_of_detection_of_circulating_melanoma_cells_A_comparative_overview.html

Methods of detection of circulating melanoma cells: A comparative overview

Cancer Treat Rev. 2011 Jun;37(4):284-290, Andrianos Nezos, Pavlos Msaouel, Nikolaos Pissimissis, Peter Lembessis, Antigone Sourla, Athanasios Armakolas, Helen Gogas, Alexandros J. Stratigos, Andreas D. Katsambas, Michael Koutsilieris

Abstract

Disease dissemination is the major cause of melanoma-related death. A crucial step in the metastatic process is the intravascular invasion and circulation of melanoma cells in the bloodstream with subsequent development of distant micrometastases that is initially clinically undetectable and will eventually progress into clinically apparent metastasis. Therefore, the use of molecular methods to detect circulating melanoma cells may be of value in risk stratification and clinical management of such patients. Herein, we review the currently applied techniques for the detection, isolation, enrichment and further characterization of circulating melanoma cells from peripheral blood samples in melanoma patients. Furthermore, we provide a brief overview of the various molecular markers currently being evaluated as prognostic indicators of melanoma progression.

http://oncologystat.com/journals/review_articles/AEP/Vitamin_D_and_Melanoma.html

Vitamin D and Melanoma

Ann Epidemiol. 2009 Jul;19(7):455-461, Kathleen M. Egan

Abstract

Purpose

Ultraviolet light from sunlight and other sources is the major environmental risk factor for melanoma of the skin. Humans also derive most of their vitamin D from exposure to sunlight. This article reviews current evidence that vitamin D might play a preventive role in the development of melanoma or affect tumor aggressiveness or melanoma patient outcomes.

Methods

Literature review.

Results

The vitamin D receptor has been identified in normal melanocytes as well as melanoma cell lines and primary tissue. A few studies have demonstrated relationships of functional polymorphisms in the vitamin D receptor with melanoma risk or tumor aggressiveness. Identifying an independent influence of vitamin D on melanoma risk is hampered by overwhelming confounding by the carcinogenic influence of ultraviolet radiation on skin melanocytes. Nonetheless an inverse association was suggested in a few studies with greater consumption of dairy foods or other dietary sources. Several lines of evidence are consistent with a potential influence for vitamin D on site-specific aggressiveness of skin melanomas, therapeutic response or patient survival.

Conclusion

Additional research is needed to determine whether vitamin D may have a preventive role in melanoma incidence or a salutary influence on melanoma patient outcome.

http://www.youtube.com/watch?v=KOUR9JSmY3w&feature

Connection with Vitamin D and Cancer

http://articles.mercola.com/sites/articles/archive/2011/11/20/deadly-melanoma-not-due-vitamin-d-deficiency.aspx

The Surprising Cause of Melanoma (And No, it's Not Too Much Sun) Posted By Dr. Mercola | November 20 2011 

http://mercola.fileburst.com/PDF/ExpertInterviewTranscripts/InterviewCaroleBaggerlyVitaminD.pdf

A Special Interview with Carole Baggerly  By Dr. Mercola on Vitamin D and Cancer

http://oncologystat.com/journals/review_articles/SOC/Surgical_Approach_to_Primary_Cutaneous_Melanoma.html

Surgical Approach to Primary Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):39-56, Patrick A. Ott, Russell S. Berman

Abstract

The surgical management of primary cutaneous melanoma, from the diagnostic biopsy through the wide local excision and nodal staging, must be carefully planned, and the biology of the melanoma, microstaging and primary tumor pathologic features of the melanoma, location on the body, patient preferences, and comorbidities must be considered. The treating surgeon must balance preservation of oncologic principles, with optimization of functional and aesthetic outcome. This article reviews the rationale behind the surgical approach in the patient with a primary melanoma.

http://oncologystat.com/journals/ew/YSDIA/Falsepositive_cells_in_sentinel_lymph_nodes.html

False-positive cells in sentinel lymph nodes

Semin Diagn Pathol. 2008 May;25(2):116-119, Jeoffry B. Brennick, Shaofeng Yan

Melanoma sentinel lymph nodes (SLN) are carefully evaluated to maximize sensitivity. Examination includes hematoxylin and eosin (H+E) stained sections at multiple levels through the node, with subsequent immunohistochemical (IHC) stains for melanocytic markers if H+E sections are negative for melanoma. However, not all IHC-positive cells in SLN are metastatic melanoma, as evidenced by the presence of MART-1 positive cells in SLN from breast cancer patients with no history of melanoma (so-called ‘false-positive’ cells). These ‘false-positive cells’ could be nodal nevus, non-melanocytic cells with cross-reacting antigenic determinants, phagocytic cells containing melanocyte antigens, or possibly melanocytes or melanocyte stem cells liberated at the time of biopsy of the cutaneous melanoma. Examination of SLN requires careful correlation of H+E and IHC findings.

http://oncologystat.com/journals/review_articles/SOC/Staging_and_Prognosis_of_Cutaneous_Melanoma.html

Staging and Prognosis of Cutaneous Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):1-17, Paxton V. Dickson, Jeffrey E. Gershenwald

Abstract

Staging of cutaneous melanoma continues to evolve through identification and rigorous analysis of potential prognostic factors. In 1998, the American Joint Committee on Cancer (AJCC) Melanoma Staging Committee developed the AJCC melanoma staging database, an international integrated compilation of prospectively accumulated melanoma outcome data from several centers and clinical trial cooperative groups. Analysis of this database resulted in major revisions to the TNM staging system reflected in the sixth edition of the AJCC Cancer Staging Manual published in 2002. More recently, the committee's analysis of an updated melanoma staging database, including prospective data on more than 50,000 patients, led to staging revisions adopted in the seventh edition of the AJCC Cancer Staging Manual published in 2009. This article highlights these revisions, reviews relevant prognostic factors and their impact on staging, and discusses emerging tools that will likely affect future staging systems and clinical practice.

http://oncologystat.com/journals/review_articles/SOC/EvidenceBased_Followup_for_the_Patient_with_Melanoma.html

Evidence-Based Follow-up for the Patient with Melanoma

Surg Oncol Clin N Am. 2011 Jan;20(1):181-200, Ryan C. Fields, Daniel G. Coit

Abstract

This article reviews the best evidence available to guide the follow-up of patients with melanoma, focusing on incidence of, and detection of, melanoma recurrence, frequency of follow-up visits, yield of, laboratory and radiographic tests, outcomes of patients with recurrent melanoma based on method of detection, detection of secondary melanomas, and stage-specific follow-up.

http://www.surgonc.theclinics.com/article/S1055-3207(10)00091-8/ppt

Immunotherapy of Melanoma: An Update

·       Jade Homsi, MD, Joshua C. Grimm, BA, Patrick Hwu, MD

     The incidence of melanoma has been increasing worldwide. A relationship between melanoma and the immune system was established years ago. Modulating the immune system in the management of different stages of melanoma has been the focus of numerous large randomized trials worldwide. This article reviews the current status of immunotherapy for melanoma, with a focus on the recent promising results from using vaccines, cytotoxic T-lymphocyte antigen-4 (CTLA-4) antibodies, and adoptive cell therapy.

http://www.ncbi.nlm.nih.gov/pubmed/18022553

Surg Oncol Clin N Am. 2007 Oct;16(4):945-73, xi.

Current immunotherapeutic strategies in malignant melanoma.

Agostino NM, Ali A, Nair SG, Mosca PJ.

Source

Department of Internal Medicine, Lehigh Valley Hospital and Health Network, 1240 South Cedar Crest Boulevard, Allentown, PA 18103, USA.

Abstract

The basis of immunotherapy for melanoma is the existence of melanoma-associated antigens that can be targeted by the immune system. Identification of many of these antigens has enabled investigators to develop a wide array of immunotherapy strategies for the treatment of melanoma. Although several of these strategies have been shown to induce antitumor immune responses in some patients, robust clinical responses have been observed less frequently. With exciting recent advancements in this field, however, there is promise of generating potent immunologic responses and translating them more consistently into durable clinical responses. This article reviews several current approaches to immunotherapy for melanoma and describes the key role that surgeons play in advancing this area of oncology.

http://www.oncologystat.com/journals/journal_scans/Ulceration_and_Stage_Are_Predictive_of_Interferon_Efficacy_In_Melanoma_Results_of_the_Phase_III_Adjuvant_Trials_EORTC_18952_and_EORTC_18991.html 

Ulceration and Stage Are Predictive of Interferon Efficacy In Melanoma: Results of the Phase III Adjuvant Trials EORTC 18952 and EORTC 18991

Breast. 2011 Oct 1;20(3), AMM Eggermont, S Suciu, A Testori, A Spatz, et al

TAKE-HOME MESSAGE

This combined analysis of two large prospective trials of adjuvant interferon for treatment of patients with resected melanoma demonstrated that tumor stage and ulceration predict for immunotherapy benefit.

Abstract

Summary: Adjuvant interferon has modest activity in melanoma patients at high risk for relapse. Patient selection is important; stage and ulceration of the primary tumour are key prognostic factors.

Methods: In this post hoc meta-analysis of European Organisation for Research and Treatment of Cancer (EORTC) trials 18952 (intermediate doses of interferon α-2b [IFN] versus observation in stage IIb-III patients) and 18991 (pegylated [PEG]-IFN versus observation in stage III patients), the predictive value of ulceration on the efficacy of IFN/PEG-IFN with regard to relapse-free survival (RFS), distant metastasis-free survival (DMFS), and overall survival (OS) was assessed in the overall population and in subgroups stratified by stage (IIb and III-N1 [microscopic nodal disease] and III-N2 [macroscopic nodal disease]).

Findings: In the overall population, the comparison of IFN/PEG-IFN versus observation for RFS, DMFS and OS yielded estimated hazard ratios (HR) of 0.85 (p=0.004), 0.89 (p=0.04) and 0.94 (p=0.36), respectively. The impact of treatment was greater in the ulceration group (n=849) compared with the non-ulceration group (n=1336) for RFS (test for interaction: p=0.02), DMFS (p<0.001) and OS (p<0.001). The greatest risk reductions were observed in patients with ulceration and stage IIb/III-N1, with estimated HR for RFS, DMFS, and OS of 0.69 (p=0.003), 0.59 (p<0.0001) and 0.58 (p<0.0001), respectively. The efficacy of IFN/PEG-IFN was lower in stage III-N2 patients with ulceration and uniformly absent in patients without ulceration. There was consistency between the data of both trials.

Interpretation: This meta-analysis of the EORTC 18952 and 18991 trials indicated that both tumour stage and ulceration were predictive factors for the efficacy of adjuvant IFN/PEG-IFN therapy.

http://oncologystat.com/journals/review_articles/archive/Metastatic_Melanoma_An_AJCC_Review.html

or  

http://www.communityoncology.net/co/journal/articles/0508441.pdf

Metastatic Melanoma: An AJCC Review

Community Oncology. 2008 Aug 1;5(8):441-445, SS Agarwala

Abstract

Outside clinical trials, current therapeutic options for patients with metastatic melanoma appear to be of limited benefit. Combination chemotherapy has not been shown to improve outcomes over single-agent chemotherapy, and dacarbazine, which is still the only agent approved by the US Food and Drug Administration for this disease, has produced low response rates and little meaningful improvement in survival. However, with the development and testing of several new compounds, both in the area of immunotherapy and targeted therapy, the future for patients with this disease may become brighter.

News Story: Investigational TKI Active Against Advanced Melanoma in Early Trial »

News Story: Tremelimumab Monotherapy Adds No Benefit Over Chemo in Metastatic Melanoma »

Journal Article: Treatment of Metastatic Melanoma With Autologous CD4+ T Cells Against NY-ESO-1 »

Journal Article: Biochemotherapy for the Treatment of Metastatic Malignant Melanoma: A Systematic Review »

Journal Article: Treatments for Metastatic Melanoma: Synthesis of Evidence From Randomized Trials »

Journal Article: Chemotherapy Compared With Biochemotherapy for the Treatment of Metastatic Melanoma: A Meta-analysis of 18 Trials Involving 2,621 Patients »

http://oncologystat.com/journals/review_articles/HOC/Progress_in_Melanoma_Histopathology_and_Diagnosis.html

Progress in Melanoma Histopathology and Diagnosis

Hematol Oncol Clin North Am. 2009 Jun;23(3):467-480, Adriano Piris, Martin C. Mihm

Abstract

The past 15 years have seen rapid advances in both our understanding of hereditary melanoma genetics and the technologies that enable scientists to make discoveries. Despite great efforts by many groups worldwide, other high-risk melanoma loci besides CDKN2A still remain elusive. A panel of polymorphisms that appears to confer low-to-moderate risk for melanoma has been assembled through functional and genome-wide association studies. The goal of personalized melanoma risk prediction is within our reach, although true clinical use has yet to be established.

http://oncologystat.com/news/Melanoma_Field_Cells_May_Explain_Local_Tumor_Recurrence_US.html  Melanoma Field Cells May Explain Local Tumor Recurrence

Elsevier Global Medical News. 2009 Mar 2, B Jancin  MAUI, HAWAII (EGMN) – The recent discovery of an entity called melanoma field cells that are often present in seemingly normal skin surrounding primary melanomas could ultimately force an overhaul of standard recommended excision margins.

These melanoma field cells are morphologically normal junctional melanocytes and thus cannot be identified using histopathologic criteria. Yet they are genetically melanoma as demonstrated using comparative genomic hybridization and fluorescent in situ hybridization, Dr. Maxwell A. Fung explained at the annual Hawaii Dermatology Seminar sponsored by the Skin Disease Education Foundation.

http://ebm.rsmjournals.com/content/234/8/825.full.pdf+html?sid=658bdab7-e25a-4654-bb4c-ac0d3900cbda

Experimental Biology and Medicine

Molecular Targets of Nutraceuticals Derived from Dietary Spices: Potential Role in Suppression of Inflammation and Tumorigenesis

Overall our review suggests “adding spice to your life” may serve as a healthy and delicious way to ward off cancer and other chronic diseases.

http://journals.lww.com/melanomaresearch/Abstract/2007/10000/Curcumin_downregulates_the_constitutive_activity.2.aspx

Melanoma Research:

October 2007 – Volume 17 – Issue 5 – pp 274-283

doi: 10.1097/CMR.0b013e3282ed3d0e

Original Articles

Curcumin downregulates the constitutive activity of NF-[kappa]B and induces apoptosis in novel mouse melanoma cells

Abstract

Melanoma, the most deadly form of skin cancer, is very aggressive and resistant to present therapies. The transcription factor nuclear factor-kappa B (NF-κB) has been reported to be constitutively active in many types of cancer. Constitutively active NF-κB seen in melanoma likely plays a central role in cell survival and growth. We have established and characterized novel cell lines from our murine melanoma model. Here we report the constitutive activity of NF-κB in these melanoma-derived cells, as shown by electrophoretic mobility shift assay and reporter assays. We hypothesized that agents that inhibit NF-κB may also inhibit cell proliferation and may induce apoptosis in such melanoma cells. Curcumin has been shown to inhibit NF-κB activity in several cell types. In our system, curcumin selectively inhibited growth of melanoma cells, but not normal melanocytes. Curcumin induced melanoma cells to undergo apoptosis, as shown by caspase-3 activation, inversion of membrane phosphatidyl serine, and increases in cells in the sub-G₁ phase. A curcumin dose-dependent inhibition of NF-κB-driven reporter activity correlated with decreased levels of phospho-IκBα, and decreased expression of NF-κB-target genes COX-2 and cyclin D1. This study demonstrates that the use of cells from our model system can facilitate studies of signaling pathways in melanoma. We furthermore conclude that curcumin, a natural and safe compound, inhibits NF-κB activity and the expression of its downstream target genes, and also selectively induces apoptosis of melanoma cells but not normal melanocytes. These encouraging in-vitro results support further investigation of curcumin for treatment of melanoma in vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12680238

Anticancer Res. 2003 Jan-Feb;23(1A):363-98.

Anticancer potential of curcumin: preclinical and clinical studies.

Aggarwal BB, Kumar A, Bharti AC.

Cytokine Research Section, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX, USA. [email protected]

Abstract

Curcumin (diferuloylmethane) is a polyphenol derived from the plant Curcuma longa, commonly called turmeric. Extensive research over the last 50 years has indicated this polyphenol can both prevent and treat cancer. The anticancer potential of curcumin stems from its ability to suppress proliferation of a wide variety of tumor cells, down-regulate transcription factors NF-kappa B, AP-1 and Egr-1; down-regulate the expression of COX2, LOX, NOS, MMP-9, uPA, TNF, chemokines, cell surface adhesion molecules and cyclin D1; down-regulate growth factor receptors (such as EGFR and HER2); and inhibit the activity of c-Jun N-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases. In several systems, curcumin has been described as a potent antioxidant and anti-inflammatory agent. Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis. Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day. All of these studies suggest that curcumin has enormous potential in the prevention and therapy of cancer. The current review describes in detail the data supporting these studies.

http://www.experts.scival.com/wayne/pubDetail.asp?t=pm&id=15252141&amp;

Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation.

http://ur.rutgers.edu/medrel/viewArticle.html?ArticleID=49

 Rutgers, The State University of New Jersey: Curry and Cauliflower Could Halt Prostate Cancer

http://www.jcrows.com/curryfightsprostatecancer.html  

Curry fights prostate cancer, study finds

http://mss3.libraries.rutgers.edu/dlr/showfed.php?pid=rutgers-lib:25088  

Prostate cancer chemoprevention by dietary phytochemicals: 

Chemoprevention entails the use of preferably dietary agents to block or suppress the various stages of prostate carcinogenesis. Flavonoids, the essential components of fruits and vegetables can modulate transcription factor AP-1 and its upstream signaling cascades mainly ERK-MAPK and JNK-MAPK in human androgen insensitive prostate cancer (PC3) cells. Soy isoflavone concentrate can upregulate the expression of several phase II detoxifying and antioxidant genes in an NF-E2-related factor 2 (Nrf2) dependent manner. In addition to detoxifying genes, soy isoflavone concentrate can also modulate the expression of genes such as LATS2, GREB1, calpain and many more in an Nrf2 dependent manner. 

In one such transgenic model, curcumin or PEITC suppressed high grade PIN levels. However a combination of low doses of these agents worked remarkably well in suppressing tumors all together.

http://www.newswise.com/articles/view/573327/

Genetic Evidence That Antioxidants Can Help Treat Cancer  

“Now we have genetic proof that mitochondrial oxidative stress is important for driving tumor growth,” said lead researcher Michael P. Lisanti, M.D., Ph.D., professor of cancer biology at Jefferson Medical College of Thomas Jefferson University and member of the Kimmel Cancer Center at Jefferson. “This means we need to make anti-cancer drugs that specially target this type of oxidative stress. And there are already antioxidant drugs out there on the market as dietary supplements, like N-acetyl cysteine.” 

The researchers report that the loss of Cav-1 increases mitochondrial oxidative stress in the tumor stroma, increasing both tumor mass and tumor volume by four-fold, without any increase in tumor angiogenesis.

“Antioxidants have been associated with cancer reducing effects—beta carotene, for example—but the mechanisms, the genetic evidence, has been lacking,” Dr. Lisanti said. “This study provides the necessary genetic evidence that reducing oxidative stress in the body will decrease tumor growth.”

 These findings were originally published in the online February 15 issue of Cancer Biology & Therapy.

http://cancerres.aacrjournals.org/content/71/13/4484

A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.

http://www.newswise.com/articles/view/574151/?sc=mwhn

Biologists Show How Veggies Work in Cancer-Fighting Diet

Released: 3/7/2011 3:00 PM EST 

Source: University of Alabama at Birmingham

Newswise — BIRMINGHAM, Ala. – Mothers around the world now collectively can say, “I told you so.”

Your vegetables are good for you, says a research review published by scientists from the University of Alabama at Birmingham in the journal Clinical Epigenetics.

In particular, vegetables such as broccoli and cabbage are filled with compounds that could help reverse or prevent cancers and other aging-related diseases as part of the “epigenetics diet,” a new lifestyle concept coined after the article’s publication.

“Your mother always told you to eat your vegetables, and she was right,” says co-author Trygve Tollefsbol, Ph.D., D.O., a biology professor in the UAB College of Arts and Sciences. “But now we better understand why she was right — compounds in many of these foods suppress gene aberrations that over time cause fatal diseases.”

Epigenetics is the study of the changes in human gene expressions with time, changes that can cause cancer and Alzheimer’s, among other diseases. In recent years, epigenetics research worldwide, including numerous studies conducted at UAB, have identified specific food compounds that inhibit negative epigenetic effects.

Those foods include soybeans, cauliflower, broccoli and cabbage. Green tea, fava beans, kale, grapes and the spice turmeric round out the diet.

“The epigenetics diet can be adopted easily, because the concentrations of the compounds needed for a positive effect are readily achievable,” says lead author Syed Meeran, Ph.D., a research assistant professor in Tollefsbol’s UAB Department of Biology laboratory.

For example, Meeran says sipping tea compounds called polyphenols in daily amounts that are equivalent to approximately three cups of green tea has been shown to reverse breast cancer in laboratory mice by suppressing the gene that triggers the disease. Similarly, a daily cup of broccoli sprouts, which has sulforaphane as an active compound, has been shown to reduce the risk of developing many cancers.

“Our review article has drawn everything together from global studies, and the common theme is that compounds in the epigenetics diet foods can, at the very least, help us lead healthier lives and help our bodies prevent potentially debilitating diseases like breast cancer and Alzheimer’s,” Tollefsbol says.

http://www.nature.com/onc/journal/v24/n48/abs/1208874a.html

Oncogene (2005) 24, 7180–7189. doi:10.1038/sj.onc.1208874; published online 11 July 2005

Luteolin induces apoptosis via death receptor 5 upregulation in human malignant tumor cells

http://www.clearviewcancer.com/index.php/newswire/details/542  Clearview Cancer Institute  

Gene maps to transform scientists' work on cancer  

The studies by international scientists and Britain's Wellcome Trust Sanger Institute are the first comprehensive descriptions of tumour cell mutations and lay bare all the genetic changes behind melanoma skin cancer and lung cancer.

AND FINALLY, IODINE DO INDEED CURE SKIN CANCER AS ADVOCATED BY DR. SIMONCINI, so keep your hopes intact, keep an open mind and do your own research. I have given you just a little bit of what is available out there without really getting into what is known as "Alternative Treatments" or "Natural Treatments".

Meanwhile read this blog, one just like yours here, written by those who has been there helping those who just ventured into the skin cancer world and see how they CURED their cancer for good:

http://www.topicalinfo.org/forum/topic.asp?TOPIC_ID=409

I am pasting just a small part of the blog below.. Click the link and read the whole thing and see for yourself. Remember the mind, like a parachute functions only when open!

As I said on the start, when it comes to cancer, you do not want to play roulette but to use ALL methods available to catch the cancer in the cross fire at the same time.

With my best to you all,

Dennis (malenomabegone)

Went to see my dermatologist a week ago ago to check up on 2 spots on my back. He took one look at what I was treating and wanted to take it out. Since it had been so much smaller I let him do it. Pathology came back yesterday that there was no invasion into the underlying layer and a lot of apoptosis, meaning cell death. My dermatologist said he had the pathologist specially look out for it after I told him what and why I was doing. Apparently the pathologist remarked that there was an "unusually high degree of apoptosis" compared to what he usually see. I am continuing my sodium bicarbonate and iodine (aqueous base) for another round to make sure nothing comes back as they normally do with surgery.

Went to see my dermatologist a week ago ago to check up on 2 spots on my back. He took one look at what I was treating and wanted to take it out. Since it had been so much smaller I let him do it. Pathology came back yesterday that there was no invasion into the underlying layer and a lot of apoptosis, meaning cell death. My dermatologist said he had the pathologist specially look out for it after I told him what and why I was doing. Apparently the pathologist remarked that there was an "unusually high degree of apoptosis" compared to what he usually see. I am continuing my sodium bicarbonate and iodine (aqueous base) for another round to make sure nothing comes back as they normally do with surgery.

Went to see my dermatologist a week ago ago to check up on 2 spots on my back. He took one look at what I was treating and wanted to take it out. Since it had been so much smaller I let him do it. Pathology came back yesterday that there was no invasion into the underlying layer and a lot of apoptosis, meaning cell death. My dermatologist said he had the pathologist specially look out for it after I told him what and why I was doing. Apparently the pathologist remarked that there was an "unusually high degree of apoptosis" compared to what he usually see. I am continuing my sodium bicarbonate and iodine (aqueous base) for another round to make sure nothing comes back as they normally do with surgery.

Please see my new post.

Dennis (melanomabegone)

Please see my new post.

Dennis (melanomabegone)

Please see my new post.

Dennis (melanomabegone)

I hate to blow your mind that cancer CAN be cured sometimes with something very simple.

Reminds me of the fable of two frogs at the bottom of the well looking up at the sky. One frog said to the other: "I know everything out there because I have seen it all" not knowing that the sky she saw and that she thought she knew so well was only a minuscule portion of what is actually out there but that was ALL that she could see.

So brace yourself for yet another bombshell for you because when it comes to curing non-melanoma skin cancer, eggplants comes to the rescue. 

http://www.bionational.com/pdf/503-514.pdf

Research Journal of Biological Sciences 2 (4): 503-514, 2007

Solasodine Rhamnosyl Glycosides Specifically Bind Cancer Cell Receptors and Induce Apoptosis and Necrosis. Treatment for Sikn Cancer and Hope for Internal Cancers

http://www.naturalnews.com/027506_eggplant_skin_cancer.html

http://www.bionational.com/library_pages/article-016-Curaderm_History.html

The History of Curaderm

Curaderm-BEC5 is intended to specifically treat:

• Basal Cell Carcinomas (BCC)
• Squamous Cell Carcinomas (SCC)
• Keratoses
• Keratoacanthomas
• Sun spots

References:

Punjabi, S., I. Cook, P. Kersey, R. Marks, A. Finlay, G. Sharpe, et al. 2000. A double blind, multi-centre parallel group study of BEC-5 cream in basal cell carcinoma. Eur. Acad. Dermatol. Venereol. 14:47-60.

Cerio, R. and S. Punjabi, 2002. Clinical appraisal of BEC5. Barts and the London NHS.

Cham, B. E., B. Daunter and R. Evans, 1992. Topical treatment of malignant and premalignant skin cancers by very low concentrations of a standard mixture of salasodine glycosides. Clin. Digest Series Dermatol., 1992.

Cham, B.E., 1994. Saloasodine glycosides as anti-cancer agents: Pre-clinical and clinical studies. Asia Pacif. J. Pharmacol., 9:113-118.

AND FROM THE JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY:

http://pubs.acs.org/doi/abs/10.1021/jf062204q

Antiangiogenic Activity of Brown Algae Fucoxanthin and Its Deacetylated Product, Fucoxanthinol

J. Agric. Food Chem., 2006, 54 (26), pp 9805–9810

DOI: 10.1021/jf062204q

Publication Date (Web): December 20, 2006

Abstract

The antiangiogenic effects of fucoxanthin and a deacetylated product, fucoxanthinol, were examined. Fucoxanthin significantly suppressed HUVEC proliferation and tube formation at more than 10 μM, but it had no significant effect on HUVEC chemotaxis. The formation of blood vessel-like structures from CD31-positive cells was evaluated using embryonic stem cell-derived embryoid bodies. Fucoxanthin effectively suppressed the development of these structures at 10−20 μM, suggesting that it could suppress differentiation of endothelial progenitor cells into endothelial cells involving new blood vessel formation. Fucoxanthin and fucoxanthinol suppressed microvessel outgrowth in an ex vivo angiogenesis assay using a rat aortic ring, in a dose-dependent manner. These results imply that fucoxanthin having antiangiogenic activity might be useful in preventing angiogenesis-related diseases.

http://pubs.acs.org/doi/abs/10.1021/jf801322m

Structures and Antioxidant Activity of Anthocyanins in Many Accessions of Eggplant and Its Related Species

J. Agric. Food Chem., 2008, 56 (21), pp 10154–10159

DOI: 10.1021/jf801322m

Publication Date (Web): October 3, 2008

Abstract

Anthocyanins were detected in extracts from the peels of 123 accessions of eggplant (Solanum melongena) and its related species. Their anthocyanin profiles were classified into four types, including known Japanese eggplant type (type 1) and non-Japanese eggplant type (type 2). Although most of the eggplant accessions had one of the two known profiles, one accession had a novel profile (type 3). Two accessions of related species showed another novel profile (type 4). The major anthocyanins were identified as delphinidin 3-(p-coumaroylrutinoside)-5-glucoside (nasunin) (type 1), delphinidin 3-rutinoside (type 2), delphinidin 3-glucoside (type 3), and petunidin 3-(p-coumaroylrutinoside)-5-glucoside (petunidin 3RGc5G) (type 4). Delphinidin 3-caffeoylrutinoside-5-glucoside (delphinidin 3RGcaf5G) was isolated from the hybrid (F1) plants of a type 1 cultivar and a type 3 germplasm. Among the five purified anthocyanins, delphinidin 3RGcaf5G showed the highest radical-scavenging activities toward both 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and linoleic acid radical, followed in order by nasunin and petunidin 3RGc5G.

http://pubs.acs.org/doi/abs/10.1021/jf050796r

Antiangiogenic Activity of Nasunin, an Antioxidant Anthocyanin, in Eggplant Peels

J. Agric. Food Chem., 2005, 53 (16), pp 6272–6275

DOI: 10.1021/jf050796r

Publication Date (Web): July 7, 2005

Abstract

Nasunin, delphinidin-3-(p-coumaroylrutinoside)-5-glucoside, an antioxidant anthocyanin isolated from eggplant peels, was demonstrated as an angiogenesis inhibitor. Nasunin at higher 10 μM suppressed microvessel outgrowth in an ex vivo angiogenesis assay using a rat aortic ring. The effect of nasunin was examined in various in vitro angiogenesis models using human umbilical vein endothelial cells (HUVECs). Nasunin suppressed HUVEC proliferation in a dose-dependent manner (50−200 μM); however, it had no significant effect on HUVEC chemotaxis in a Boyden chamber assay and HUVEC tube formation on a reconstituted basement membrane. These results imply that nasunin with both antioxidant and antiangiogenic activities might be useful to prevent angiogenesis-related diseases.

http://pubs.acs.org/doi/abs/10.1021/jf801322m

Structures and Antioxidant Activity of Anthocyanins in Many Accessions of Eggplant and Its Related Species

J. Agric. Food Chem., 2008, 56 (21), pp 10154–10159

DOI: 10.1021/jf801322m

Publication Date (Web): October 3, 2008

Abstract

Anthocyanins were detected in extracts from the peels of 123 accessions of eggplant (Solanum melongena) and its related species. Their anthocyanin profiles were classified into four types, including known Japanese eggplant type (type 1) and non-Japanese eggplant type (type 2). Although most of the eggplant accessions had one of the two known profiles, one accession had a novel profile (type 3). Two accessions of related species showed another novel profile (type 4). The major anthocyanins were identified as delphinidin 3-(p-coumaroylrutinoside)-5-glucoside (nasunin) (type 1), delphinidin 3-rutinoside (type 2), delphinidin 3-glucoside (type 3), and petunidin 3-(p-coumaroylrutinoside)-5-glucoside (petunidin 3RGc5G) (type 4). Delphinidin 3-caffeoylrutinoside-5-glucoside (delphinidin 3RGcaf5G) was isolated from the hybrid (F1) plants of a type 1 cultivar and a type 3 germplasm. Among the five purified anthocyanins, delphinidin 3RGcaf5G showed the highest radical-scavenging activities toward both 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and linoleic acid radical, followed in order by nasunin and petunidin 3RGc5G.

 http://pubs.acs.org/doi/abs/10.1021/jf051841y

Nasunin from Eggplant Consists of Cis−Trans Isomers of Delphinidin 3-[4-(p-Coumaroyl)-l-rhamnosyl (1→6)glucopyranoside]-5-glucopyranoside

J. Agric. Food Chem., 2005, 53 (24), pp 9472–9477

DOI: 10.1021/jf051841y

Publication Date (Web): November 1, 2005

Abstract

Two major anthocyanins were isolated from the acidified methanolic extract of eggplant (Solanum melongena L.) by column chromatography and preparative high-performance liquid chromatography. These anthocyanins were interconvertible under room light illumination condition. By means of tandem time-of-flight mass spectrometry and nuclear magnetic resonance spectroscopy, their structures were identified and elucidated as delphinidin 3-[4-(cis-p-coumaroyl)-l-rhamnosyl(1→6)glucopyranoside]-5-glucopyranoside (compound 1) and delphinidin 3-[4-(trans-p-coumaroyl)-l-rhamnosyl-(1→6)glucopyranoside]-5-glucopyranoside (compound 2), respectively. The results indicated that nasunin comprised cis and trans isomers of the p-coumaric acid moiety in its structure.

I hope the above information is not too "confusing" for you as per your post. While it is uplifting to see the support for each other for what you are all going through or have gone through in this blog, it is also depressing to see that it appears that all the participants just sit there letting their oncologist do whatever without realising that beating cancer is a team effort between the oncologist and the patient. There are a lot you can do to not only effect a better outcome and suffer less side effects but also to maxomize the chance that the cancer does not returm. Here we are talking about your life style, your diet, supplements of vitamins, antioxidants as well as spices especially curcumin as I had posted earlier. More so is that when you are proactive doing your part and empowering yourself to be responsible for your health and to fight the cancer you don't feel as helpless and depressed as opposed to just sitting there "taking it" which will make for a less optimum outcome. Your emotional and psychological well being DOES affect the progress and outcome of yout treatment. Don't take my word for it. Ask your doctor!

Good luck to you all and good bye.

Dennis (melanomabegone)

I hate to blow your mind that cancer CAN be cured sometimes with something very simple.

Reminds me of the fable of two frogs at the bottom of the well looking up at the sky. One frog said to the other: "I know everything out there because I have seen it all" not knowing that the sky she saw and that she thought she knew so well was only a minuscule portion of what is actually out there but that was ALL that she could see.

So brace yourself for yet another bombshell for you because when it comes to curing non-melanoma skin cancer, eggplants comes to the rescue. 

http://www.bionational.com/pdf/503-514.pdf

Research Journal of Biological Sciences 2 (4): 503-514, 2007

Solasodine Rhamnosyl Glycosides Specifically Bind Cancer Cell Receptors and Induce Apoptosis and Necrosis. Treatment for Sikn Cancer and Hope for Internal Cancers

http://www.naturalnews.com/027506_eggplant_skin_cancer.html

http://www.bionational.com/library_pages/article-016-Curaderm_History.html

The History of Curaderm

Curaderm-BEC5 is intended to specifically treat:

• Basal Cell Carcinomas (BCC)
• Squamous Cell Carcinomas (SCC)
• Keratoses
• Keratoacanthomas
• Sun spots

References:

Punjabi, S., I. Cook, P. Kersey, R. Marks, A. Finlay, G. Sharpe, et al. 2000. A double blind, multi-centre parallel group study of BEC-5 cream in basal cell carcinoma. Eur. Acad. Dermatol. Venereol. 14:47-60.

Cerio, R. and S. Punjabi, 2002. Clinical appraisal of BEC5. Barts and the London NHS.

Cham, B. E., B. Daunter and R. Evans, 1992. Topical treatment of malignant and premalignant skin cancers by very low concentrations of a standard mixture of salasodine glycosides. Clin. Digest Series Dermatol., 1992.

Cham, B.E., 1994. Saloasodine glycosides as anti-cancer agents: Pre-clinical and clinical studies. Asia Pacif. J. Pharmacol., 9:113-118.

AND FROM THE JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY:

http://pubs.acs.org/doi/abs/10.1021/jf062204q

Antiangiogenic Activity of Brown Algae Fucoxanthin and Its Deacetylated Product, Fucoxanthinol

J. Agric. Food Chem., 2006, 54 (26), pp 9805–9810

DOI: 10.1021/jf062204q

Publication Date (Web): December 20, 2006

Abstract

The antiangiogenic effects of fucoxanthin and a deacetylated product, fucoxanthinol, were examined. Fucoxanthin significantly suppressed HUVEC proliferation and tube formation at more than 10 μM, but it had no significant effect on HUVEC chemotaxis. The formation of blood vessel-like structures from CD31-positive cells was evaluated using embryonic stem cell-derived embryoid bodies. Fucoxanthin effectively suppressed the development of these structures at 10−20 μM, suggesting that it could suppress differentiation of endothelial progenitor cells into endothelial cells involving new blood vessel formation. Fucoxanthin and fucoxanthinol suppressed microvessel outgrowth in an ex vivo angiogenesis assay using a rat aortic ring, in a dose-dependent manner. These results imply that fucoxanthin having antiangiogenic activity might be useful in preventing angiogenesis-related diseases.

http://pubs.acs.org/doi/abs/10.1021/jf801322m

Structures and Antioxidant Activity of Anthocyanins in Many Accessions of Eggplant and Its Related Species

J. Agric. Food Chem., 2008, 56 (21), pp 10154–10159

DOI: 10.1021/jf801322m

Publication Date (Web): October 3, 2008

Abstract

Anthocyanins were detected in extracts from the peels of 123 accessions of eggplant (Solanum melongena) and its related species. Their anthocyanin profiles were classified into four types, including known Japanese eggplant type (type 1) and non-Japanese eggplant type (type 2). Although most of the eggplant accessions had one of the two known profiles, one accession had a novel profile (type 3). Two accessions of related species showed another novel profile (type 4). The major anthocyanins were identified as delphinidin 3-(p-coumaroylrutinoside)-5-glucoside (nasunin) (type 1), delphinidin 3-rutinoside (type 2), delphinidin 3-glucoside (type 3), and petunidin 3-(p-coumaroylrutinoside)-5-glucoside (petunidin 3RGc5G) (type 4). Delphinidin 3-caffeoylrutinoside-5-glucoside (delphinidin 3RGcaf5G) was isolated from the hybrid (F1) plants of a type 1 cultivar and a type 3 germplasm. Among the five purified anthocyanins, delphinidin 3RGcaf5G showed the highest radical-scavenging activities toward both 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and linoleic acid radical, followed in order by nasunin and petunidin 3RGc5G.

http://pubs.acs.org/doi/abs/10.1021/jf050796r

Antiangiogenic Activity of Nasunin, an Antioxidant Anthocyanin, in Eggplant Peels

J. Agric. Food Chem., 2005, 53 (16), pp 6272–6275

DOI: 10.1021/jf050796r

Publication Date (Web): July 7, 2005

Abstract

Nasunin, delphinidin-3-(p-coumaroylrutinoside)-5-glucoside, an antioxidant anthocyanin isolated from eggplant peels, was demonstrated as an angiogenesis inhibitor. Nasunin at higher 10 μM suppressed microvessel outgrowth in an ex vivo angiogenesis assay using a rat aortic ring. The effect of nasunin was examined in various in vitro angiogenesis models using human umbilical vein endothelial cells (HUVECs). Nasunin suppressed HUVEC proliferation in a dose-dependent manner (50−200 μM); however, it had no significant effect on HUVEC chemotaxis in a Boyden chamber assay and HUVEC tube formation on a reconstituted basement membrane. These results imply that nasunin with both antioxidant and antiangiogenic activities might be useful to prevent angiogenesis-related diseases.

http://pubs.acs.org/doi/abs/10.1021/jf801322m

Structures and Antioxidant Activity of Anthocyanins in Many Accessions of Eggplant and Its Related Species

J. Agric. Food Chem., 2008, 56 (21), pp 10154–10159

DOI: 10.1021/jf801322m

Publication Date (Web): October 3, 2008

Abstract

Anthocyanins were detected in extracts from the peels of 123 accessions of eggplant (Solanum melongena) and its related species. Their anthocyanin profiles were classified into four types, including known Japanese eggplant type (type 1) and non-Japanese eggplant type (type 2). Although most of the eggplant accessions had one of the two known profiles, one accession had a novel profile (type 3). Two accessions of related species showed another novel profile (type 4). The major anthocyanins were identified as delphinidin 3-(p-coumaroylrutinoside)-5-glucoside (nasunin) (type 1), delphinidin 3-rutinoside (type 2), delphinidin 3-glucoside (type 3), and petunidin 3-(p-coumaroylrutinoside)-5-glucoside (petunidin 3RGc5G) (type 4). Delphinidin 3-caffeoylrutinoside-5-glucoside (delphinidin 3RGcaf5G) was isolated from the hybrid (F1) plants of a type 1 cultivar and a type 3 germplasm. Among the five purified anthocyanins, delphinidin 3RGcaf5G showed the highest radical-scavenging activities toward both 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and linoleic acid radical, followed in order by nasunin and petunidin 3RGc5G.

 http://pubs.acs.org/doi/abs/10.1021/jf051841y

Nasunin from Eggplant Consists of Cis−Trans Isomers of Delphinidin 3-[4-(p-Coumaroyl)-l-rhamnosyl (1→6)glucopyranoside]-5-glucopyranoside

J. Agric. Food Chem., 2005, 53 (24), pp 9472–9477

DOI: 10.1021/jf051841y

Publication Date (Web): November 1, 2005

Abstract

Two major anthocyanins were isolated from the acidified methanolic extract of eggplant (Solanum melongena L.) by column chromatography and preparative high-performance liquid chromatography. These anthocyanins were interconvertible under room light illumination condition. By means of tandem time-of-flight mass spectrometry and nuclear magnetic resonance spectroscopy, their structures were identified and elucidated as delphinidin 3-[4-(cis-p-coumaroyl)-l-rhamnosyl(1→6)glucopyranoside]-5-glucopyranoside (compound 1) and delphinidin 3-[4-(trans-p-coumaroyl)-l-rhamnosyl-(1→6)glucopyranoside]-5-glucopyranoside (compound 2), respectively. The results indicated that nasunin comprised cis and trans isomers of the p-coumaric acid moiety in its structure.

I hope the above information is not too "confusing" for you as per your post. While it is uplifting to see the support for each other for what you are all going through or have gone through in this blog, it is also depressing to see that it appears that all the participants just sit there letting their oncologist do whatever without realising that beating cancer is a team effort between the oncologist and the patient. There are a lot you can do to not only effect a better outcome and suffer less side effects but also to maxomize the chance that the cancer does not returm. Here we are talking about your life style, your diet, supplements of vitamins, antioxidants as well as spices especially curcumin as I had posted earlier. More so is that when you are proactive doing your part and empowering yourself to be responsible for your health and to fight the cancer you don't feel as helpless and depressed as opposed to just sitting there "taking it" which will make for a less optimum outcome. Your emotional and psychological well being DOES affect the progress and outcome of yout treatment. Don't take my word for it. Ask your doctor!

Good luck to you all and good bye.

Dennis (melanomabegone)

I hate to blow your mind that cancer CAN be cured sometimes with something very simple.

Reminds me of the fable of two frogs at the bottom of the well looking up at the sky. One frog said to the other: "I know everything out there because I have seen it all" not knowing that the sky she saw and that she thought she knew so well was only a minuscule portion of what is actually out there but that was ALL that she could see.

So brace yourself for yet another bombshell for you because when it comes to curing non-melanoma skin cancer, eggplants comes to the rescue. 

http://www.bionational.com/pdf/503-514.pdf

Research Journal of Biological Sciences 2 (4): 503-514, 2007

Solasodine Rhamnosyl Glycosides Specifically Bind Cancer Cell Receptors and Induce Apoptosis and Necrosis. Treatment for Sikn Cancer and Hope for Internal Cancers

http://www.naturalnews.com/027506_eggplant_skin_cancer.html

http://www.bionational.com/library_pages/article-016-Curaderm_History.html

The History of Curaderm

Curaderm-BEC5 is intended to specifically treat:

• Basal Cell Carcinomas (BCC)
• Squamous Cell Carcinomas (SCC)
• Keratoses
• Keratoacanthomas
• Sun spots

References:

Punjabi, S., I. Cook, P. Kersey, R. Marks, A. Finlay, G. Sharpe, et al. 2000. A double blind, multi-centre parallel group study of BEC-5 cream in basal cell carcinoma. Eur. Acad. Dermatol. Venereol. 14:47-60.

Cerio, R. and S. Punjabi, 2002. Clinical appraisal of BEC5. Barts and the London NHS.

Cham, B. E., B. Daunter and R. Evans, 1992. Topical treatment of malignant and premalignant skin cancers by very low concentrations of a standard mixture of salasodine glycosides. Clin. Digest Series Dermatol., 1992.

Cham, B.E., 1994. Saloasodine glycosides as anti-cancer agents: Pre-clinical and clinical studies. Asia Pacif. J. Pharmacol., 9:113-118.

AND FROM THE JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY:

http://pubs.acs.org/doi/abs/10.1021/jf062204q

Antiangiogenic Activity of Brown Algae Fucoxanthin and Its Deacetylated Product, Fucoxanthinol

J. Agric. Food Chem., 2006, 54 (26), pp 9805–9810

DOI: 10.1021/jf062204q

Publication Date (Web): December 20, 2006

Abstract

The antiangiogenic effects of fucoxanthin and a deacetylated product, fucoxanthinol, were examined. Fucoxanthin significantly suppressed HUVEC proliferation and tube formation at more than 10 μM, but it had no significant effect on HUVEC chemotaxis. The formation of blood vessel-like structures from CD31-positive cells was evaluated using embryonic stem cell-derived embryoid bodies. Fucoxanthin effectively suppressed the development of these structures at 10−20 μM, suggesting that it could suppress differentiation of endothelial progenitor cells into endothelial cells involving new blood vessel formation. Fucoxanthin and fucoxanthinol suppressed microvessel outgrowth in an ex vivo angiogenesis assay using a rat aortic ring, in a dose-dependent manner. These results imply that fucoxanthin having antiangiogenic activity might be useful in preventing angiogenesis-related diseases.

http://pubs.acs.org/doi/abs/10.1021/jf801322m

Structures and Antioxidant Activity of Anthocyanins in Many Accessions of Eggplant and Its Related Species

J. Agric. Food Chem., 2008, 56 (21), pp 10154–10159

DOI: 10.1021/jf801322m

Publication Date (Web): October 3, 2008

Abstract

Anthocyanins were detected in extracts from the peels of 123 accessions of eggplant (Solanum melongena) and its related species. Their anthocyanin profiles were classified into four types, including known Japanese eggplant type (type 1) and non-Japanese eggplant type (type 2). Although most of the eggplant accessions had one of the two known profiles, one accession had a novel profile (type 3). Two accessions of related species showed another novel profile (type 4). The major anthocyanins were identified as delphinidin 3-(p-coumaroylrutinoside)-5-glucoside (nasunin) (type 1), delphinidin 3-rutinoside (type 2), delphinidin 3-glucoside (type 3), and petunidin 3-(p-coumaroylrutinoside)-5-glucoside (petunidin 3RGc5G) (type 4). Delphinidin 3-caffeoylrutinoside-5-glucoside (delphinidin 3RGcaf5G) was isolated from the hybrid (F1) plants of a type 1 cultivar and a type 3 germplasm. Among the five purified anthocyanins, delphinidin 3RGcaf5G showed the highest radical-scavenging activities toward both 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and linoleic acid radical, followed in order by nasunin and petunidin 3RGc5G.

http://pubs.acs.org/doi/abs/10.1021/jf050796r

Antiangiogenic Activity of Nasunin, an Antioxidant Anthocyanin, in Eggplant Peels

J. Agric. Food Chem., 2005, 53 (16), pp 6272–6275

DOI: 10.1021/jf050796r

Publication Date (Web): July 7, 2005

Abstract

Nasunin, delphinidin-3-(p-coumaroylrutinoside)-5-glucoside, an antioxidant anthocyanin isolated from eggplant peels, was demonstrated as an angiogenesis inhibitor. Nasunin at higher 10 μM suppressed microvessel outgrowth in an ex vivo angiogenesis assay using a rat aortic ring. The effect of nasunin was examined in various in vitro angiogenesis models using human umbilical vein endothelial cells (HUVECs). Nasunin suppressed HUVEC proliferation in a dose-dependent manner (50−200 μM); however, it had no significant effect on HUVEC chemotaxis in a Boyden chamber assay and HUVEC tube formation on a reconstituted basement membrane. These results imply that nasunin with both antioxidant and antiangiogenic activities might be useful to prevent angiogenesis-related diseases.

http://pubs.acs.org/doi/abs/10.1021/jf801322m

Structures and Antioxidant Activity of Anthocyanins in Many Accessions of Eggplant and Its Related Species

J. Agric. Food Chem., 2008, 56 (21), pp 10154–10159

DOI: 10.1021/jf801322m

Publication Date (Web): October 3, 2008

Abstract

Anthocyanins were detected in extracts from the peels of 123 accessions of eggplant (Solanum melongena) and its related species. Their anthocyanin profiles were classified into four types, including known Japanese eggplant type (type 1) and non-Japanese eggplant type (type 2). Although most of the eggplant accessions had one of the two known profiles, one accession had a novel profile (type 3). Two accessions of related species showed another novel profile (type 4). The major anthocyanins were identified as delphinidin 3-(p-coumaroylrutinoside)-5-glucoside (nasunin) (type 1), delphinidin 3-rutinoside (type 2), delphinidin 3-glucoside (type 3), and petunidin 3-(p-coumaroylrutinoside)-5-glucoside (petunidin 3RGc5G) (type 4). Delphinidin 3-caffeoylrutinoside-5-glucoside (delphinidin 3RGcaf5G) was isolated from the hybrid (F1) plants of a type 1 cultivar and a type 3 germplasm. Among the five purified anthocyanins, delphinidin 3RGcaf5G showed the highest radical-scavenging activities toward both 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and linoleic acid radical, followed in order by nasunin and petunidin 3RGc5G.

 http://pubs.acs.org/doi/abs/10.1021/jf051841y

Nasunin from Eggplant Consists of Cis−Trans Isomers of Delphinidin 3-[4-(p-Coumaroyl)-l-rhamnosyl (1→6)glucopyranoside]-5-glucopyranoside

J. Agric. Food Chem., 2005, 53 (24), pp 9472–9477

DOI: 10.1021/jf051841y

Publication Date (Web): November 1, 2005

Abstract

Two major anthocyanins were isolated from the acidified methanolic extract of eggplant (Solanum melongena L.) by column chromatography and preparative high-performance liquid chromatography. These anthocyanins were interconvertible under room light illumination condition. By means of tandem time-of-flight mass spectrometry and nuclear magnetic resonance spectroscopy, their structures were identified and elucidated as delphinidin 3-[4-(cis-p-coumaroyl)-l-rhamnosyl(1→6)glucopyranoside]-5-glucopyranoside (compound 1) and delphinidin 3-[4-(trans-p-coumaroyl)-l-rhamnosyl-(1→6)glucopyranoside]-5-glucopyranoside (compound 2), respectively. The results indicated that nasunin comprised cis and trans isomers of the p-coumaric acid moiety in its structure.

I hope the above information is not too "confusing" for you as per your post. While it is uplifting to see the support for each other for what you are all going through or have gone through in this blog, it is also depressing to see that it appears that all the participants just sit there letting their oncologist do whatever without realising that beating cancer is a team effort between the oncologist and the patient. There are a lot you can do to not only effect a better outcome and suffer less side effects but also to maxomize the chance that the cancer does not returm. Here we are talking about your life style, your diet, supplements of vitamins, antioxidants as well as spices especially curcumin as I had posted earlier. More so is that when you are proactive doing your part and empowering yourself to be responsible for your health and to fight the cancer you don't feel as helpless and depressed as opposed to just sitting there "taking it" which will make for a less optimum outcome. Your emotional and psychological well being DOES affect the progress and outcome of yout treatment. Don't take my word for it. Ask your doctor!

Good luck to you all and good bye.

Dennis (melanomabegone)

Thanks all for your input. I have uploaded my photos to http://melanomabegone.shutterfly.com/

Your opinion is appreciated. My treatment continues then to see my dermatologist. 

Thanks. Dennis

Thanks all for your input. I have uploaded my photos to http://melanomabegone.shutterfly.com/

Your opinion is appreciated. My treatment continues then to see my dermatologist. 

Thanks. Dennis

Thanks all for your input. I have uploaded my photos to http://melanomabegone.shutterfly.com/

Your opinion is appreciated. My treatment continues then to see my dermatologist. 

Thanks. Dennis