MPIP: Melanoma Patients Information Page

The MPIP is the oldest and largest community of people affected by melanoma hosted through the Melanoma Research Foundation. It is designed to provide support and information to caregivers, patients, family and friends. Once you have been touched by melanoma—either as a patient or as a family member or friend of a patient—you become part of a community. It is not a community anyone joins willingly. But if you must be part of this group, you will find no better place to find the tools you need in your journey with this cancer, and the friends who can make that journey more bearable.

The information on the bulletin board is open and accessible to everyone. To add a new topic or to post a reply, you must be a registered user. Please note that you will be able to post both topics and replies anonymously even though you are logged in. All posts must abide by MRF posting policies.

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carol b's picture
Replies 7
Last reply 1/23/2011 - 11:33am

my pet scans just showed only the tumors we can see and feel..NO mets anwhere eles in my body. THANK GOD FOR THAT

Believe all thing are possible, believe faith can move mountains, believe in the healing power of prayer and never ever give up on your dreams

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nickmac56's picture
Replies 18
Last reply 9/17/2012 - 11:26pm

My wife is Stage 4 with tumors on lung being monitored as part of her clinical trial on Ipi.  Has had a number of subcutaneous tumors removed.  Is getting her 12 week scan next Tuesday, but we know Ipi hasn't worked, yet, because minimally she has some new ones on her back and stomach.  We suppose it's possible that there may be some effect between week 12 and week 16 scan - anyone else seen reductions during this timeframe?  Our oncologist is terrific and there is great care here in Seattle, but we are running out of options.  One thing we apparently will try next week is a permanent regimen of Tamoxofin  - to shut down her hormone system because in the past there has been some weak linkage to hormones and melanoma - any one else gone this route?  Lastly, assuming Ipi failure, has anyone then gone on to IL-2?  She started off with Leukine which got her onto the clinical trial when she had a reaction to it.

thanks for any help or suggestions,  Nick

Her motto: "Don't wait for the storm to pass, love dancing in the rain".

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Anonymous's picture
Replies 2
Last reply 1/27/2011 - 6:59am

Hi,

 

I am new to the MPIP site & been reading everything. I am stage 3, unrescetable Braf positive. My doctor says I qualify for Braf or Braf/MEK combo trial.

Would like to know for anyone what kind of side effectss and timeframe for a response (tumor shrinkage) have you experienced.

Also, if you get "remission"/no more tumors do you still have to kep taking the drugs forever???

I am scared and hope to learn more from you so that I can go into the trial with realistic expectations.

Any feedback on your experience would be greatly appreciated.

God Bless you all

Lena

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molly's picture
Replies 2
Last reply 1/22/2011 - 10:07am
Replies by: molly, Anonymous

Does anyone know of a board like this for Prostate Cancer?

Thank you so much,

molly

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jlevang's picture
Replies 2
Last reply 1/28/2013 - 10:36pm
Replies by: mkt, Carver

I'm new to this forum, and new to the world of melanoma. I was diagnosed with a stage 2a melanoma on my thigh in Dec. and had the wide excision and sentinel node biopsy done on 12/31. The nodes came back negative, which was a huge relief, and now I'm trying to educate myself on what I should be doing to prevent reoccurences. Recovery is mostly going well, except for a large lump that developed around the incision near the groin where the lymph nodes came out. There is one firm lump at the top of the incision, and then a larger one running most of the length of the 5" incision. The surgeon said it is likely a seroma, and that he could aspirate and drain it, but that they often come back. He recommends letting it go away on its own, which he said can take weeks or months. I'm hoping someone has gone through this, and has advice, or information about how long it takes, what to do, etc.  I'm having a hard time finding much information about seromas, especially in the groin area. Sounds like they are more common in the armpits. It's not really painful just uncomfortable. Thanks.

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Shelby - MRF's picture
Replies 8
Last reply 1/21/2011 - 9:03pm

Can you spare a few minutes to take a survey?

Synovate Healthcare is a medical and healthcare market research firm.  They are conducting a market research project and would like to ask for your assistance.  This is an opportunity to offer your insight and perspective regarding treatment for metastatic melanoma.  To complete the survey, you will first be asked a few qualifying questions.  In return for completing the 25 minute survey, Synovate Healthcare is offering $35 for your time and a donation to the MRF.

Synovate Healthcare will keep all of your answers completely confidential and results will only be reported as a whole – not as individual responses.  Please note that when you click over to the survey, you will be redirected to the Synovate Healthcare site.  The survey is done online.

If you’ve been diagnosed with melanoma and are interested in participating, please use this link:

https://mr01.equesta2.net/mrIWeb/mrIWeb.dll?I.Project=U55J8EMAILADD&i.user2=Advocacy1 

Once you have completed the survey, there will be a page to specify where you would like your honoraria sent. Your participation is enormously helpful! 

Shelby - MRF

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Nebr78's picture
Replies 3
Last reply 1/21/2011 - 11:39pm
Replies by: SusanE, Lori C, sharmon

i am waiting to evaluate 2 golf ball size lumps on my face and chest.  I had 7-8 strong doses of radiation and if they begin to shrink He will give them some more zaps..Strong chemo is out of the question as I have serious heart disease.

What I am having trouble facing is if the lumps don't shrink, there is nothing more that can be done.

How long might it be before the tumors kill me?  And will it be done slow or fast.?

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Nebr78's picture
Replies 1
Last reply 1/20/2011 - 8:40pm
Replies by: W.

Has anyone had any bumps, lumps on their body and had them treated with radiation?   If so, did it work.   I have 2 lumps (tumors), one on side of face and another in front of right arm pit.  They gave me 7-8 strong radiation treatments a few days ago. Nothing is new except the one on the face hurts like the devil unless i take pain pills.   Is Melanoma resistant to Radiation you think.     Retired in Nebraska

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Linda J's picture
Replies 1
Last reply 1/20/2011 - 9:21pm
Replies by: King

So the new plan is to get at the ones in my brain with WBR starting Monday. That will last for 5 days and then I'll be doing carbo and taxol until I can get on braf trial that also targets the brain. That study is coming to Canada in about six weeks.
I'm wondering if other people have had experience with carbo and taxol.
I believe that God has a plan of healing in my life. There is still hope in the midst of what seems to be extreme darkness night now.
Linda J

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Anonymous's picture
Anonymous
Replies 0

Interesting article in the Guardian about what they are finding in the BRAF trials in the UK.

http://www.dailymail.co.uk/health/article-1348793/Skin-cancer-A-pill-fight-disease-year-

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Kim K's picture
Replies 7
Last reply 1/21/2011 - 9:53am

I guess it is about time finally (after prodding my docs).  Brain MRI, PET/CT whole body, CT chest without and with contrast.  For some reason they only wanted to CT the chest, as if mel dosen't like to go to the liver, GI tract or anywhere else in the abdomen/pelvis.  At least I won't have to drink the nasty contrast this time.  I am getting over a stomach bug and don't want to revisit cherry flavored chalk.  I didn't push too hard on the abdo. CT figuring that if anything was there, the PET/CT should pick it up.

My main goal for this visit is to get a scanning schedule down on paper so all my docs are on the same page.

Take care all!

Cancer Sucks Shit Happens Nothing is ever 100% bad, there is a reason and silver lining in everything. Sometimes I need a good light and my glasses to find it though. You can't fix stupid.

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Hawaii Bob's picture
Replies 1
Last reply 1/20/2011 - 5:57am
Replies by: Kim K

This past summer saw a revolution in melanoma therapy. Patients whose melanoma lesions contain a mutation in the BRAF gene were successfully treated with a BRAF-specific inhibitor, PLX4032. Reports of the drug trial described shrinking tumors and improved health. Yet seven months after therapy began the tumors returned and resumed growing. Now, scientists at The Wistar Institute explain why: the tumor learns to signal around the blocked gene by adjusting its molecular wiring. They also show how to overcome resistance by simultaneously targeting multiple signaling pathways.

The researchers see this as further evidence that some cancers must be treated with multiple targeted drugs at the outset of treatment. Their findings are published in the December 14 issue of the journal Cancer Cell.

"The evidence suggests that targeting mutant BRAF can kill cancer cells, but it is not enough by itself to finish off melanoma," said Meenhard Herlyn, D.V.M., D.Sc., director of The Wistar Institute Melanoma Research Center and leader of Wistar's Molecular and Cellular Oncogenesis program. "The good news is that drugs are being developed to work in combination with BRAF inhibitors, which our data clearly shows is our best option if we intend to beat advanced melanoma."

Melanoma is the deadliest, most aggressive form of skin cancer. While surgical treatment of early melanoma leads to 90 percent cure rates, advanced melanoma is notoriously resistant to chemotherapy and has a tendency to metastasize, or spread, throughout the body. According to the World Health Organization, cases of the disease continue to rise, which has helped spur research into therapies such as BRAF inhibitors.

To study how melanoma responds to BRAF inhibitors, the Herlyn lab took melanoma cells with the BRAF mutation and tested them against a variety of anti-mutant BRAF drugs. When exposed to the drugs, the cells died off dramatically only to grow back again. In fact, cells that became resistant to one type of BRAF drug became resistant to all of them, which suggests that the cells were biochemically "rewired" in such a way that they no longer needed BRAF to form tumors.

"Cells are complex machines that work, essentially, through chains of biochemical reactions that we refer to as signaling pathways," said Jessie Villanueva, Ph.D., senior author on the study and staff scientist in the Herlyn laboratory. "Knocking out mutant BRAF shuts a major pathway down, but if some cells can use an alternate pathway, then they can survive."

To find out which alternate pathways the drug-resistant cells use, Villanueva and her colleagues looked for signs of increased activation among proteins along the pathways BRAF uses, as well as other pathways.

Their hunt turned up two paths that worked together to aid survival. First, they found that resistant cells used a protein similar to BRAF to carry the signal down the chain. Second, they found these cells received an additional boost from the IGF-1 receptor, a protein that sits on the surface of cells and sends signals that prevent cells from being killed. The resistant cells re-route the signal around BRAF by switching to an alternate protein (CRAF or ARAF), which promotes tumor cell growth, while IGF-1R signaling promotes survival of the resistant cells.

Fortunately, there are a number compounds in clinical development that could block signals along both these pathways. So-called MEK inhibitors target a protein along the same pathway as BRAF, and IGF-1 receptor inhibitors (and inhibitors of P13K, a protein that can be activated by the IGF-1 receptor pathway) block the cancer-enabling survival signal. To test these drug combinations in the BRAF-inhibitor resistant cells, the Herlyn laboratory used a tool they developed to simulate the real-world environment of human cells: 3-D melanoma tumor spheroids. Their 3-D tissue cultures allow melanoma cells to grow in all directions, much like a new melanoma tumor would grow after metastasis. As predicted, a combination of these two inhibitors killed BRAF-resistant melanoma cells in the Wistar 3-D model.

Moreover, the Herlyn laboratory confirmed in tissue samples from patients in the PLX4032 trial taken both before treatment and after they developed resistance that an increased expression of the IGF-1 receptor is associated with resistance to BRAF inhibitors. None of the laboratory-generated cell lines or the post-relapse patient's tumor samples analyzed had new mutations in the BRAF, NRAS, or c-Kit genes.

Additionally, the researchers noted an association between the loss of a tumor suppressor called PTEN, and resistance to BRAF inhibitors in melanoma cell lines. The scientists found that the relapsed tumor of one patient included in the study lost the PTEN gene, even though it was present before treatment. These findings suggest that loss of PTEN could be an additional way that melanoma cells gain resistance to BRAF inhibitors. The Wistar group continues to investigate these and other mechanisms of resistance, as they expect that several will likely arise given the heterogeneous nature of melanoma.

"Tumors are efficient engines of evolution they are going to find a way around most treatments, so we want to kill all the malignant cells from the very beginning," said Villanueva. "By targeting both pathways simultaneously you hit these cells with two punches from which they cannot recover."

"If you do this at the outset of treatment, we reason, it will prevent melanoma survival and hopefully improve patient outcomes," Villanueva added.

Support for this study was provided by grants from the National Cancer Institute and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation.

Wistar co-authors in this study include Adina Vultur, Ph.D.; John T. Lee, Ph.D.; Rajasekharan Somasundaram, Ph.D.; Mizuho Fukunaga-Kalabis, M.D., Ph.D.; Angela K. Cipolla; James E. Hayden; and Ademi E. Santiago-Walker, Ph.D. University of Pennsylvania School of Medicine co-authors include Katherine L. Nathanson, M.D.; Xiaowei Xu, M.D., Ph.D.; Phyllis A. Gimotty, Ph.D.; Bradley Wubbenhorst; Richard Letrero; Kurt D'Andrea; and Anitha Pushparajan. Other authors included Grant A. McArthur, M.B., B.S., Ph.D.; and Damien Kee, MBBS, FRACP, of the Peter MacCallum Cancer Centre in Victoria, Australia; Jeffrey A. Sosman, M.D., and Kimberly Dahlman Brown of the Vanderbilt University Medical Center; and Sylvie Laquerre, Ph.D., of GlaxoSmithKline's division of Oncology Biology in Collegeville, Pa.

Source: Wistar Institute

 

Article URL: http://www.medicalnewstoday.com/articles/211315.php

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Not sure if this qualifies as a "major breakthroug" as the original article's title states, but it is interesting and adds to the community's base of knowledge about melanoma genetics ...... Hawaii Bob, Stage IIA, Oahu, USA.......BTW, from the website "MedicalNewsToday" ......

Link at the bottom......

In a breakthrough that could lead to new treatments for patients with malignant melanoma, researchers from Mount Sinai School of Medicine have discovered that a particular protein suppresses the progression of melanoma through regulation of an oncogene, or gene responsible for cancer growth. The study is published in Nature.

Researchers studied the natural progression of melanoma using mouse and human cells, as well as patient samples and determined that the presence of a specific histone variant, which is a protein that helps package DNA, was directly related to the growth of melanoma. In all instances, researchers observed that as the melanoma became more aggressive, the presence of the histone variant macroH2A decreased. Researchers then manipulated macroH2A levels in melanoma and found that when they removed it in the early stages of the disease, the melanoma progressed more aggressively both in growth and metastasis. Adding macroH2A to late-stage aggressive melanoma cells created the opposite effect.

"We wanted to determine whether macroH2A is a passenger in this process or if it's crucial in the progression of melanoma," said Emily Bernstein, PhD, Assistant Professor of Oncological Sciences and Dermatology, Mount Sinai School of Medicine, and lead author of the study. When further investigating macroH2A function in melanoma, the researchers found that it regulates CDK8, a known oncogene for colorectal cancer. "CDK8 is highly expressed in aggressive melanoma, suggesting it also plays a major role in the process," Dr. Bernstein explained.

Through further functional studies, researchers found that eliminating macroH2A led to an increase in CDK8 expression, and the elimination of CDK8 in metastatic melanoma cells impaired their proliferation. These results suggest that macroH2A suppresses melanoma progression, at least in part, through the regulation of CDK8.

"Very little is known about melanoma epigenetics or the histone-mediated epigenetic changes in cancer in general, so these findings are a major step forward in our research. As we move ahead, we would like to determine how to inhibit CDK8 function, thereby inhibiting the growth of melanoma, as well as identify additional epigenetic changes in melanoma progression." said Dr. Bernstein. "What these discoveries really highlight is the need for further studies into the epigenetic code of cancer."

 

http://www.medicalnewstoday.com/articles/212399.php

 

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New US National Comprehensive Cancer Network Guidelines for Melanoma Patients
"The National Comprehensive Cancer Network® (NCCN®) aims to provide people with cancer and the general public state-of-the-art cancer treatment information in easy-to-understand language. The NCCN Guidelines for Patients™, based on the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines™), are meant to help you when you talk with your doctor about treatment options that are best for you. These guidelines do not replace the expertise and clinical judgment of your doctor.

NCCN is pleased to present the new NCCN Guidelines for Patients™ on Melanoma. This 72 page PDF file is available for download at the link below. I believe newly diagnosed patients will find this booklet to be a very valuable source in understanding their specific melanoma, treatment options, etc., in a handy, "one stop shop" format.....

V/R

Hawaii Bob
Stage IIA
NED 2 years & 5 months (but who's counting)

http://www.nccn.com/images/patient-g...f/melanoma.pdf

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LynnLuc's picture
Replies 5
Last reply 1/20/2011 - 1:45pm

I wanted to share this..it was released today...http://www.nih.gov/news/health/jan2011/nci-19.htm

 

Embargoed for Release
Wednesday, January 19, 2011
1 p.m. EST

Contact:
NCI Office of Media Relations
301-496-6641

NIH study in mice uncovers pathway critical for UV-induced melanoma

Scientists have made an unanticipated discovery in mice that interferon-gamma, a type of protein primarily used by the immune system for intercellular communication, acts as a promoter for the deadly form of skin cancer known as melanoma. This finding resulted from a series of experiments designed to understand how solar ultraviolet (UV) radiation causes melanoma. The results of this study suggest that interferon-gamma, which has been thought to contribute to an innate defense system against cancer, under some circumstances may promote melanoma and incite the development of tumors. The work, led by researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, appeared online in Nature, Jan. 19, 2011.

Cutaneous melanoma is a highly aggressive and frequently drug-resistant cancer with rising incidence rates. The major environmental risk factor for melanoma is UV radiation exposure, usually from the sun, with the highest risk associated with intermittent burning doses, especially during childhood.

Over the past 10 years, the researchers used genetically engineered mice first to prove, and then to try to understand, the connection between exposure to UV radiation and the initiation of melanoma. The current work was the latest attempt to define the molecular mechanisms of this cause and effect relationship. The results of this study offer the possibility that the inhibition of interferon-gamma immediately after sunburn might block the carcinogenic activation of the skin’s pigment-producing cells, known as melanocytes, making it a potentially effective preventive strategy against UV radiation-induced melanoma, according to the scientists.

The key to the experiments, led by Glenn Merlino, Ph.D., Laboratory of Cancer Biology and Genetics, NCI, and research fellow and first author M. Raza Zaidi, Ph.D., was the development of a unique genetically engineered mouse in which the melanocytes were exclusively labeled with a green fluorescent protein. This fluorescent tag allowed visual tracking and specific purification of melanocytes from the mouse skin. For the first time this enabled researchers to evaluate the response of melanocytes to UV radiation exposure while residing in the natural skin environment of a living animal.

The researchers observed that UV radiation doses equivalent to what would cause sunburn in human skin resulted in increased numbers and movement of melanocytes within the mouse skin. A detailed analysis of gene expression changes associated with this melanocyte activation revealed abnormal expression of a number of genes known to be responsive to interferon-gamma.

When the function of interferon-gamma was inhibited at the time of UV radiation, the number of melanocytes and their movement remained normal, suggesting that interferon-gamma was responsible for the UV radiation-induced activation of the melanocytes.

The source of interferon-gamma within the skin was determined to be macrophages — cells that normally protect against infection — that had infiltrated the skin after UV exposure. The pro-melanoma potential of these macrophages was revealed when they were found to enhance the growth of melanomas when transplanted under the skin of mice.

This effect was abolished when interferon-gamma was blocked, corroborating its importance in promoting melanoma development. Moreover, when the scientists examined human melanoma tissue samples, they found interferon-gamma-producing macrophages in 70 percent of the tumors, supporting the idea that these macrophages can significantly contribute to the initiation and/or progression of human melanoma.

"We anticipate that this discovery may change how interferons are used in the clinic as anticancer agents," said Merlino. "Our findings raise the possibility that targeting the interferon-gamma pathway may represent a novel, less toxic therapeutic alternative for effective treatment of malignant melanoma patients, who currently have poor cure rates."

These studies were made possible through long-term collaborations with Edward De Fabo, Ph.D., and Frances Noonan, Ph.D., of George Washington University Medical Center, Washington, D.C.

NCI leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at www.cancer.gov or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

Reference: Zaidi MR, et al., Interferon-gamma links ultraviolet radiation to melanomagenesis in mice, Nature, Jan. 27, 2010, DOI: 10.1038/nature09666.

 

 

Advocate for your own treatment.. Stage 4 Melanoma NED Surgery,Radiation, Temodar 300Mg July 2009-March 2010, then Thorocotomy...now "Phase I Study of Anti-PD-1 Human Monoclonal Antibody MDX-1106 and Vaccine Therapy"

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