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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Vermont_Donna's picture
Replies 14
Last reply 11/23/2011 - 4:54pm


Had Round two of Ipi yesterday. My oncologist thought he saw some pigmentation changes in my skin (looked me over with a blacklight) and he said that was encouraging. Also he did agree that all my melanomas (2 dozen or so) on my leg and the sub-q's are all bigger ie inflamed and that if we are thinking on the hopeful side this would be a good sign as tumors get inflamed before withering away.....of course the dark side would be I have more melanomas and the ones I have are bigger and growing. But we are going to choose to think positively! The infusion went well, I fell asleep again and my ffriend who drove me and my mom knitted and chatted away. once awake I had a reiki session and some lunch! Everyone is so positive and so warm but professional too!

My wounds are not cleaning up that well with the enzymatic debrider (Santyl) but we are going to try one more week before going to surgical debridement. I am having more pain in my calf and cant lay my leg on the bed to sleep, have to lay on my side with pillows between my legs to give "space" between my calves....cant have anything touch my calf as the wounds are too painful and throbbing. My oncologist drew two lines around one of the round the really red part and the second one further out, around where the redness ends. If the redness exceeds the lines I am to go to two of my antibiotics a day instead of one and call him.

So thats the update. Wishing you a very Merry Christmas and Happy Holiday for those who dont celebrate Christmas.


stage 3a, have done many different treatments, currently doing an clinical trial of "Ipi"

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Anonymous's picture
Replies 9
Last reply 11/23/2011 - 4:33pm

Hello!  My father was diagnosed with melanoma (on top of his head) 12yrs ago.  He had surgery to remove and was told if he made it 5yrs without recurrence he should be "in the clear".  Unfortunately, last month he began having abdominal pain and weakness which resulted in him being hospitalized.  While there a CT was performed which revealed recurrence of the melanoma.  He has mets to an area beside of his kidney, a lesion in his omentum and positive lymph nodes in his chest.   He has malignant melanoma (BRAF V600 mutation).  He began the drug Zelboraf today.  I'm very interested in speaking to anyone that may  have information about this medication (side effects, response rate, etc). 

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KT's picture
Replies 4
Last reply 11/23/2011 - 4:20pm
Replies by: dearfoam, KT, jmmm

Hi- I've read posts here from time to time... diagnosed stage 3A last year and have been seeing the folks at MDA. This year I've become short of breath, on oxygen, weak, etc. The scans are mostly clear except a couple of lung nodules and some other random "spots" they are watching in my pelvis. I'm a "healthy" 26 year old. They scheduled me for a wedge resection of the left lung to get to the bottom of things because I continue to decline. It's weird, I think. My question for you all is regarding the surgery... like how was the recovery and the chest tube, the pain, etc. - when I ask my doctors they make it seem somewhat serious... anyone who has been through it? Thank you so much!!!

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deirgey's picture
Replies 9
Last reply 11/23/2011 - 4:12pm
Replies by: Anonymous, sharmon, deirgey, Jim in Denver, LynnLuc, lhaley

My father has tested negative for the most common gene mutations, BRAF and KIT.  We were hoping for one of these b/c we were under the assumption that there are more treatment options available with either of the 2.  He has Melanoma in his spine, liver and lungs.  It took about 4 weeks for the tests to come back and we finally got them today.  His doctor recommended he start treatment next week with Abraxine (chemo drug) and Avastin b/c we don't know the gene mutation but he needs treatment ASAP.   Just looking for advice, comments, suggestions?  Anybody else in a similar situation? 

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I had a craniotomy Nov 1 and SRS on 3rd brain tumor Nov 10.  In the past three days I am experiencing really bad headaches.  Should I be worried?  


Thanks, David

“There are only two ways to live your life. One is as though nothing is a miracle. The other is as though everything is a miracle.” ― Albert Einstein

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Replies by: lhaley

Just updating you all from last week. It turns out, my brain tumor was just a figment of my imagination as my MRI was clear. My blood work did show that I am a bit anemic, although the docs didn't think anything needed to be done in regards to that. I will be going back in for CT and blood work in 14 days after a quick visit to Costa Rica and we should have a much better idea of how the Yervoy is working. Thanks for all the support.

Also, I don't know if he ever posted here or not, but Mike Brockey passed away just a few days ago. He was a true warrior. He wrote the blog sMelanoma Cancer Stinks, which my wife and I read, more her than me. Even though I never wrote to him or met him, he was an influence on my family, and for that I am grateful. He was just 33.


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It's been over a week since I had gamma knife on 2 brain mets (2.5cm and one was .7mm).  I never had any symptoms.

I know gamma knife is quite successful, but I'm scared that the radiation isn't going to stop this from growing.  I think I have at least an 80% chance of this stableizing or shrinking and just want to know what other people know.  My radiologist said the small one would probably vanish, but the larger one would probably shrink and turn into a dead mass, but not necessarily disappear.

Since my scans arn't until January, it makes me scared waiting that long - especially if it's growing.  However, the radiologist said there's a downside to imaging and that it's too soon to see what's happening. 

From reading other people's stories about gamma knife, the majority of people's either disappeared, shrunk or was stable, I havn't read anybody's story of the gamma knife not working, so that has to be a good thing.



Many impossible things have been accomplished for those who refuse to quit

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TracyLee's picture
Replies 5
Last reply 11/23/2011 - 1:45am

Hi y'all,

Still hanging in, trying to make it to 12/1 without another lung drain. Has anyone done Zelboraf in combo with Temodar?

Side effects, even just on Temodar? Tips? I'm sorry, I know there are posts for Temodar, but I'm too tired to try and find them. I'm still working full time, not sleeping well at all.

BUT, I'm here, and I have so much to be thankful for. Those long, sleepless nights, I pray and list all the small and large joys of each day.

Praying for us all!



Never will I leave you, never will I forsake you. Hebrews 13:5 Cast all your anxiety on Him, because He cares. 1 Peter 5:7 Stage IV 5/16/11 Ipi - 4 rounds May - July 2011 BRAF expanded access trial 8/8/11

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boot2aboot's picture
Replies 1
Last reply 11/23/2011 - 1:36am
Replies by: CaptAaron


Melanoma International Congress: Clinicians and Researchers Make Sense of Resistance Mechanisms

By CancerNetwork Editors | November 17, 2011
The theme of the Society for Melanoma Research (SMR) meeting in Tampa this year was “Advancement through Collaboration,” and this theme was clearly reflected. With melanoma therapies stealing the plenary session limelight two years in a row at the annual meeting of the American Society of Clinical Oncology (ASCO), with the presentation of ipilimumab in previously treated metastatic melanoma patients, and two abstract presentations: ipilimumab as a first-line treatment for metastatic melanoma, and the targeted BRAF inhibitor, vemurafenib, for first-line treatment of metastatic melanoma in patients with BRAF-mutated tumors.


Ipilimumab, approved in March of this year, was the first agent approved for metastatic melanoma in 13 years, with vemurafenib not far behind. These two drugs appear to be just the tip of the iceberg for melanoma treatment. Already, there are trials testing a combined BRAF and MEK inhibitor that will move into a phase III trial next year and, based on the partial phase I and II results, the combo is more efficacious and has lower adverse events than a single BRAF inhibitor.


Patients from clinical trials of targeted agents (and especially from the BRAF inhibitor trials) are providing important data in the form of tumor and blood samples and response rates. A major hot topic of the meeting is also the study of the mechanisms of resistance to vemurafenib.

Vemurafenib has an approximately 80% response rate within a two-month treatment cycle, with a two- to eighteen-month period of regression. However, all patients eventually develop resistance to the drug and relapse. The mechanisms of relapse are sometimes through a secondary BRAF mutation; another mutation in the same, MAPK pathway; or activation or up-regulation of an alternative survival pathway. Several papers have already been published documenting the types of novel mutations seen in patients’ resistant tumors. These analyses are ongoing along with pre-clinical research on mechanisms of resistance.


The rationale is that knowing what other genes and pathways become important upon resistance to BRAF inhibitor exposure will direct the development of unique combinations to block these pathways and prevent both resistance and disease recurrence. Researchers at the Melanoma Congress highlighted the importance of identifying the “universe” of resistance mechanisms and integrating these with clinical characterization of the disease.


The laboratory of Gavin Robertson, PhD of the Department of Pharmacology at Penn State is looking at the epigenetic changes that occur in melanoma upon BRAF inhibitor exposure using a melanoma cell model. Robertson and colleagues have found that an invasive suppressor, CD82, is both methylated and silenced upon BRAF inhibitor exposure, suggesting that a combination of BRAF and DNA demethylation targets is a potential clinical approach to overcome resistant, invasive melanoma.


Keiran Smalley, PhD of the H. Lee Moffitt Cancer Center and Research Institute and colleagues are studying a unified approach to overcome resistance based on the observation that the majority of genes implicated in vemurafenib resistance are targeted by the heatshock protein HSP90. Treating melanoma cell lines with either intrinsic or acquired resistance to vemurafenib with XL188 (veliparib), a targeted HSP90 inhibitor, resulted in inhibition of growth and survival.


The negative results of a phase II clinical trial of veliparib combined with temozolomide(Drug information on temozolomide) in late-stage metastatic melanoma patients was also reported at the meeting. These new data reinforce the common sentiment of researchers in the field that the complexity of melanoma requires combination and, potentially, sequential combination treatments. A phase I clinical trial combining a BRAF inhibitor and XL188 is currently being planned.


Rather than going on a “fishing expedition,” researchers now have the tools to create hypothesis-driven models of melanoma resistance in the laboratory. With the large number of available targeted agents, many of which have already been tested in human trials, clinical trials with the most promising combination treatments can be taken to the clinic. “The biology of late, compared to early, resistance may be different,” said Dr. Jeffrey Sosman, director of the melanoma and tumor immunotherapy program at the Vanderbilt Cancer Center in Nashville, highlighting another key area of research that needs to be pursued. The key will be the continued collaboration of laboratory researchers and clinicians

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Julie678's picture
Replies 9
Last reply 11/22/2011 - 10:55pm
Replies by: Julie678, Jessmoon, Anonymous, fdess056, LynnLuc

Hi, my husband has melanoma and we are getting conflicting opinions on radiation.  We are quickly learning there is no concensus on treatment when it comes to mel!  The brief history is my husband had a malignant mole on his back 9 years ago in 2002.  In 2002 he had a wide excision and a negative sentinel lymph node biopsy.  After 6 years of regular follow up he was let go in 2008.  This October he found a mass under his left arm-the same area as the SLNB in 2002.  On Nov 2 he had an axillary lymph node dissection.  There was only one involved node that measured 4.7cm with no extra capsulary extension.  Everything else was negative including the PET and brain CT. The surgical oncologist has a hunch that mel was missed on SLNB in 2002 and it is very possible they got it all during this surgery. The decision is ours but she thinks it would not be out of line to decline radiation due to the risk of lymphedema. We have seen a medical oncologist at Mayo and he is also very cautious about radiation.  The radiation oncologist believes radiation is worth the risk.  Any thoughts?  Mayo did recommend Leukine which we are very seriously considering.  The only other option we have found in MN is a head to head trial of IPI vs. Interferon.  We are not at all interested in Interferon and like the reduced side effects of Leukine.  Any guidance on Leukine or radiation would be greatly appreciated.

Thanks!  Julie

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marfda's picture
Replies 2
Last reply 11/22/2011 - 10:54pm
Replies by: Charlie S, lhaley

I saw a Rad Onc today after my radiation session. I am recieving radiation to my lower back for recurrent sub q tumors along my scar line. Yesterday I discovered a lump on my groin underneath my SNB scar. Showed it to the doctor today and it is concerning. He estimates it's 2-3cm wide. I am seeing my surgeon on Monday for a fine needle biopsy. It will be interesting to see what decisions will be made about surgery vs continuing radiation. I suppose since the radiation and surgery would be in two different places, I could probably technically do both at the same time. Have any of you faced an interruption of radiation? I'm also wondering when I'll have scans again. My last was in October, it was clear. Would they remove the sub q tumor even if the tumor has spread further in my body?

I know I'm assuming the lump in Melanoma. Sometimes I do better emotionally expecting the worst case scenario. 

Who shall separate us from the love of Christ? Shall tribulation, or distress, or persecution, or famine, or nakedness, or danger, or sword?... No, in all these things we are more than conquerors through him who loved us. Romans 8:35–37

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lizzykittycat's picture
Replies 6
Last reply 11/22/2011 - 8:04pm
Replies by: lizzykittycat, Charlie S, msue5, Anonymous

i fear that i'm experiencing lymphodema, but am not sure.  at this point, i've only had 2 sentinel nodes removed about a month ago.  i didn't experience the pain and swelling for about 2 weeks after the surgery.  it seemed to begin around when my (horrible) wound was debrided.  it became very "angry" and infected.  soon thereafter, i had pain starting up by my groin (dissection spot) down to my feet. 

for about the past 2 and 1/2 weeks, this pain and swelling has persisted.  i'm not sure if it can be attributed to true lymphodema because i lost those 2 nodes, or if it is a reaction to the infected excision wound.  it is tolerable, but consistent and painful.  the whole inside of my leg feels tight and hurts if i flex in different directions.  in addition, my ankle and foot is swollent non-stop.

i'm facing the lymphadenectomy in about 2 months as soon as my wound is healed to prevent infection.  i'm agonizing over the decision whether to have the surgery or not (which i've posted about previously).  the issue now is that i'm TRULY fearful of lymphodema.  if i'm experiencing it already from just the removal of 2, what do i have to anticipate after the procedure???  i feel like i'd rather not have a leg than to have to deal with this, or probably worse, for the rest of my life.

has anyone had a temporary flare up in reaction to the excision?  it was on my calf, by the way.  i have an appt with my surgical onc on mon.  i'm hoping he can provide SOME insight.  so far, he's really only said we can't tell what is going on.  :(

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boot2aboot's picture
Replies 2
Last reply 11/22/2011 - 4:01pm
Replies by: boot2aboot, TracyLee


Melanoma International Congress: Immunotherapy and Targeted Therapy Combinations Touted
By CancerNetwork Editors | November 22, 2011
Immunotherapy is finally getting the cancer clinical and research community excited:  A large portion of the presentation and discussion at the Melanoma International Congress, held in Tampa, Florida last week focused on immunotherapy approaches for the treatment of the disease. 
With the approval of the anti-CTLA4 antibody, ipilimumab, for metastatic melanoma, which has shown an overall survival of 10.1 months in a second-line trial and is now approved as both a first-line and second-line treatment for the advanced disease, the immunology field is seeing a lot more of the limelight. Academic researchers working on novel immune-harnessing treatments and vaccines are garnering more interest from the pharmaceutical industry for commercialization.
While the enthusiasm for ipilimumab from both patients and clinicians continues, there is a already anticipated excitement about a novel immunotherapy currently in early development, an antibody called anti-PD1. Both CTLA4 and PD-1 are critical immunologic checkpoints that normally function to restrain the immune system. While multiple anti-PD1 agents are in development, the one with the most patient data is BMS-96558 (MDX-1106), a potent, fully human antibody against PD-1. Phase I trials in melanoma patients as well as other cancer patients have shown promising, durable responses.
Dr. Mario Sznol, professor of medicine and co-director of the Melanoma Program at the Yale Medical School, in his presentation said anti-PD1 “is one of the most promising approaches in melanoma.” Part of that reason is that, based on the less than 50 patients for whom there is longer-term data; the immunological adverse event rates appear more muted compared to those seen with ipilimumab.
The question of whether ipilimumab, in addition to anti-PD1 treatment is more efficacious than a single agent-treatment is being addressed in a small phase I trial that's carefully looking at the best tolerated dosage in order to minimize adverse events while increasing the response rate and durability of ipililumab monotherapy. 
The congress presentations also highlighted both immunology agents and targeted treatments for melanoma. Importantly, the meeting emphasized a multi-disciplinary approach of combining these two treatments. Jedd Wolchok, MD, PhD from the Memorial Sloan Kettering Cancer Center, who was an integral part in the clinical trials that led to the approval of ipilimumab, described the rationale for combination therapy. Specifically, he discussed the combination of ipilimumab with vemurafenib, the targeted, oral BRAF inhibitor, as having the potential to achieve the balance of the high response rate of vemurafenib with the durable disease control seen with ipilimumab.
Dr. Antoni Ribas of the UCLA Jonsson Comprehensive Cancer Center presented preclinical data on the evidence that the combination may be effective. Using cell lines derived from a mouse model with a V600E mutation in BRAF, the mutation in BRAF that is targeted by vemurafenib, Dr. Ribas and his laboratory have shown that cells treated with both agents respond with apoptosis, as well as prevention of activation of the pathway components downstream of BRAF, namely the effector proteins, ERK and MEK. Importantly, the preclinical data shows that there is no effect of vemurafenib on lymphocyte viability, which is crucial for ipilimumab to achieve its effectiveness. A first in-human trial combining vemurafenib and ipillimumab in metastatic melanoma patients is scheduled to begin by 2012. The hope, according to the researchers, is that vemurafenib will increase the effectiveness of immunotherapy in part by facilitating tumor antigen presentation. The trial will also address whether the timing and rate of resistance to vemurafenib will be affected by concurrent ipilimumab therapy.
“In two years we will have our tenth anniversary. Before the IMC meetings began, there was no real galvanizing meeting that focused on melanoma research and the [Society for Melanoma Research] meeting has since evolved into the premier meeting, with the strong emphasis on research while also reaching out to our clinical colleagues. The research results from the laboratory translate very quickly into the clinics with ever increasing frequency and is a very broad effort,” said Meenhard Herlyn, Professor of Dermatology at the Wistar Institute and part of the University of Pennsylvania School of Medicine, commenting on the evolution of the annual melanoma meeting.
Looking to the future, researchers are coming together as part of the Breakthrough Consortium to begin important clinical trials, including promising combination therapies. Professor Herlyn advocates for better and more rigorous pre-clinical testing of these combinations before the start of patient trials.
“There is now a consortium established by the Melanoma Research Foundation, called the Breakthrough Consortium and this consortium has integrated 12 different institutions conducting clinical trials, with the specific goal of developing combination therapies. Both clinical trials are starting. Instead of going blindly into those clinical trials, we need more preclinical studies to carefully plan for them and so each clinical trial should have a solid rationale from pre-clinical studies. This will also be established through this consortium, which has five different sub-committees. We hope that in this way, the melanoma disease model will become the core of an adaptive, rapid learning community that provides each patient with the best possible outcome while aggregating results over all patients to advance the standard of care."
Melanoma has become a model example of a cancer for which clinical outcomes are refined based on molecular subtypes and for which there is a tremendous interaction of the melanoma clinical and research community. With many industry and academic-funded combination trials in the near future, there outcomes in the next few years should prove to be very interesting.  
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boot2aboot's picture
Replies 0


Protein linked to spread of skin cancer
Tuesday 22 November 2011


An international team of researchers working together on both sides of the Atlantic have pinpointed a protein, called P-Rex1, that seems to play a key role in the spread of malignant melanoma - the most deadly form of skin cancer, according to a paper in Nature Communications.

The team, led by researchers from the Cancer Research UK-fundedBeatson Institute of Cancer Research in Glasgow, were studying cells called melanoblasts - highly mobile cells involved in the early development of the skin.

Researchers believe that the way melanoblasts move around body tissues very similar to how melanoma cells spread. The major cause of death from melanoma is due to it spreading, or metastasising, from the initial tumour.

The discovery came when the team noticed that mice which lacked the gene that which makes the P-Rex1 protein, had skin cancers that did not spread.

Armed with this knowledge, the research team then tested human melanoma cells and tumour tissue and discovered raised levels of P-Rex1, suggesting that the protein was involved in the movement of the cells.

The discovery will give researchers a better understanding of how the cells work, which in turn enables them to better select a target for developing new treatments.

Researcher Channing Der, a member of the team based at the Lineberger Comprehensive Cancer Center the US, said: "We know that mutations in a gene called BRAF are important for the development of melanoma and several years ago we published a collaborative paper listing 82 proteins that seem to be affected by this genetic pathway. From that list, we focused on P-Rex1."

The BRAF gene was discovered to be involved in melanoma by Cancer Research UK scientists, and this year a drug - vemurafenib - was developed that targets melanomas in which the BRAF gene is defective. This is thought to be the case for around 80 per cent of patients.

The discovery that P-Rex1 is 'downstream' of BRAF - in other words, signals coming from BRAF need to 'pass through' P-Rex1 - is significant because it suggests that drugs that target P-Rex1 could - in theory - help the 20 per cent of people with melanoma whose cancer doesn't have a faulty BRAF gene.

Nell Barrie, senior science information manager at Cancer Research UK, said: "Cancer is difficult to treat once it has spread, and research that helps us to understand how cancer cells travel around the body is helping scientists to target this process with new drugs. Studies like this give us more ammunition against melanoma and other types of cancer, but it's important to remember that it can take years to turn a discovery in the lab into a treatment for patients."

Copyright Press Association 2011

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