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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Kimberly Duncan Watts's picture
Replies 5
Last reply 2/28/2012 - 1:27pm

Another question already! I was told I do not qualify for zelboraf because my BRAF gene is "abnormal". Again, that happen to anybody else?

I can do all things through Christ who strengthens me.

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Kimberly Duncan Watts's picture
Replies 8
Last reply 2/28/2012 - 1:18pm

I completed my 4th dose January 8. At my 2 wk follow up appt I was so anemic it required a double transfusion and I now am on an iron supplement. This happen to anyone else? Also, as I am the only IPI patient in my area (upstate NY) and only the 5th melanoma patient ever, my onc. Is flying blind, although he is meant to be in contact w the specialist at Roswell in Buffalo (who we spoke to this morning and for the second time, can't find that they have rec'd scans...) My first scans showed no disease in any organs, but he couldn't tell me if the lesions in my abdomen were even lesions anymore, maybe cysts, and they couldn't really read the bowel. I am rapidly losing confidence as I was diagnosed in 08 and have been thru Interferon as well as IL2 this past summer. Any advice will be greatly appreciated. I was originally told IPI was a "one-shot" deal and now I read of those of you that are rein ducted. HELP!!! I am beginning to feel these people are just not on top of my case. 53years old with 5children , 2 grandchildren and a new granddaughter literally any second now! I'm a fighter and NOT ready to pack it in!!!!

I can do all things through Christ who strengthens me.

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boot2aboot's picture
Replies 1
Last reply 2/27/2012 - 4:12pm


don't know about you, but a lot of these i have never heard of before...have to do my own research and thought it would be helpful to share.  i got this from the Aim
BRAF Inhibitors in Combination

There are several clinical trials looking at the combination of vemurafenib (Zelboraf) with the older and newer drugs. There will also be a trial testing dabrafenib in combination.


  • Vemurafenib + Ipilimumab (brand name Yervoy) is a combination of a targeted therapy and an immunotherapy in patients with the BRAF V600 mutation.


  • Vemurafenib + Bevacizumab (brand name Avastin) is a combination of a targeted therapy and an anti-angiogenic therapy.


  • Vemurafenib + BKM120 combines two targeted therapies. BKM120 is a targeted agent that inhibits a molecule called phosphatidylinositol 3-kinase (PI3K).


  • Dabrafenib + Trametinib combines a targeted therapy with a MEK inhibitor. The phase 2 study showed that the frequency of responses in the combination is similar to dabrafenib alone, but with the addition of trametinib these responses may be longer lasting with reduced side effects.  A study of dabrafenib plus trametinib versus dabrafenib plusplacebo is now in preparation.



MEK is a critical member of the MAPK pathway involved in growth and survival of cancer cells. 


  • Trametinib is a potent and highly selective inhibitor of MEK activation and kinase activity. It is now in a phase II clinical trial to investigate the objectiveresponse rate, safety, and pharmacokinetics in patients with the BRAF V600 mutation who were previously treated with a BRAF inhibitor.  


  • Selumetinib is given either as a single agent or in combination with MK-2206 (a new compound inhibiting another protein important for cancer growth called Akt). Currently the drug is being tested in melanoma patients with the BRAF V600 mutation whose disease has progressed after being treated with vemurafenib or dabrafenib.



Mutations in KIT are most frequently seen in certain melanoma subtypes, particularlyacral lentiginous melanoma (melanoma of the palms, soles, and nail beds), mucosal melanomas, as well as those melanomas associated with extensive sun damage. In those patients treatment with KIT inhibitors such as imatinib and sunitinib has been reported to be beneficial. 


  • Imatinib (brand name Gleevec) is approved for the treatment of chronic myeloid leukemia and Gastrointestinal Stromal Tumors (GIST). Tumor shrinkage has been reported in melanoma patients with KIT mutations and multiple Phase II trials are currently testing imatinib alone or in combination with chemotherapy for this group of patients. 


  • Nilotinib (brand name Tasigna) is approved for the treatment of chronic myeloid leukemia and is currently being tested in melanoma patients with KIT mutations.


  • Dasatinib (brand name Sprycel) is approved for chronic myeloid leukemia and is being tested in multiple Phase II trials for melanoma patients with KIT mutations. 


Other Targets with Potential in Melanoma

Several other pathways and targets are currently being explored in melanoma. The following is a list of some targets for which drugs are being tested in early phase clinical trials: CDK2, CDK4, and ERBB4.

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Lisa13's picture
Replies 2
Last reply 3/1/2012 - 5:55am

When I had my 28th week scan from ipi, they noticed I had marginal growth of my lung mets (1-2mm).  When my blood work was done at the end of January, my LDH was down 100 points (around 209) which is considered normal. How is this possible when my cancer has gotten a bit bigger but now my LDH is the lowest it's been since last November??   Half of me hopes that it's really inflammatio and the ipi is still working, but nobody even knows.

I just started ipi again last Friday, so let's hope this continues to work. I think there is a 30-40%,chance,  but I don't think anybody knows how well the reinduction works.  Luckily after a year, I still have lungs mets that are under 1cm and some that are just over 1cm. I also feel good knowing my absolute lymphocytes have been 1900 before I started my reinduction,  so I hope this means good things on my immune system and helps to keep the brain mets from coming back.


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

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Hi...seems there are several drugs approved for treatment of other cancers which are showing great promise in treatment of melanoma.  Is anyone aware of any of these drugs, had experience with them or investigating them?  For example, dasatinib (C-KIT inhibitor) has been approved for CML (leukemia) and is showing significant results in treatment of advanced melanoma. I am grateful for any feedback.

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Anonymous's picture
Replies 8
Last reply 2/27/2012 - 7:13pm

Hi all,

I'm 33 and have had 2 primary melanomas in the past 2.5 years, one stage 1A and one in situ. I have had two great dermatologists in different health systems both listed as melanoma centers of excellence - both of whom have left practice in Arizona for one reason or another.  I am now looking for a new team and am wondering - what training do I want my doc to have? Banner MD Anderson just opened here, but the docs listed on their website as their "melanoma specialists" were trained in hem/oncology, internal medicine and surgery. No mention of dermatology.  I assume training above and beyond what is offered in medical school is important - but maybe I'm wrong? What training is required for a good melanoma specalist? Has anyone been treated at the new AZ Banner/MD Anderson? I'd love to hear people's thoughts and experiences.

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aldakota22's picture
Replies 4
Last reply 2/27/2012 - 3:42pm

  Does anyone know of any drug trials using both new approved treatments of Zelborak & Yervoy. Was talk  late last year that such a combination was being considered for stage 4 patients. Have not seen or heard of any on going trails.

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  Does anyone know of any drug trials using both new approved treatments of Zelborak & Yervoy. Was talk  late last year that such a combination was being considered for stage 4 patients. Have not seen or heard of any on going trails.

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emmapeal's picture
Replies 2
Last reply 2/28/2012 - 7:08am
Replies by: MeNDave, runnergirl

Tari...happy 5th Angel Birthday...You are so loved....and so missed...

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beatricefromPARIS's picture
Replies 1
Last reply 2/25/2012 - 8:45pm
Replies by: FormerCaregiver


Is my hemoglobin recently rising from 10g/dl for over the last 2 years to 11.5g (nearly the 12g minimum level of ordinary women!) a good sign for my immunity?

Or is it good news for cancer cells also ie bad news for me?

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Is my hemoglobin recently rising from 10g/dl for over the last 2 years to 11.5g (nearly the 12g minimum level of ordinary women!) a good sign for my immunity?

Or is it good news for cancer cells also ie bad news for me?

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natasha's picture
Replies 1
Last reply 2/25/2012 - 12:55pm
Replies by: Janner

Hello everyone !

Thanks for all information I can find on this useful forum .

Probably I am poranoid but it is seems very odd to me ,that my Doc did not do full body check after my diagnosys.

I am diagnosed in beggining of January ,docs still deciding about Wider excision but I ever been told for appointment for full body check

I understand ,if it is one melanoma found ,it can be more developing on the same time (or am I wrong?)

I am trying to check myself ,but cannot do it everywhere and too paranoid it is melanomas all around my body :(

D docs need to do full body check straigh away afte rsurgery and how it was in your cases ?

Thanks again

Sorry for so many questions from me on the forum , because my last appointment with doctor lasted literaly 5 minutes and I even did not have a chance to ask him my questions.

All he said , - ''you should be fine with your 0.2mm and we will decide about wider excision''

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boot2aboot's picture
Replies 2
Last reply 2/27/2012 - 12:46pm
Replies by: Jeff's Mom, aldakota22




I have always thought that the more information you have , the better you can fight melanoma.   This is an excellent, UNDERSTANDABLE explanation of the MapKinese Pathway...the one zelboraf works on and the pathway that affects Braf mutated melanoma time runs out for Zelboraf effectiveness, it is good to know this because we can find trials lower down on MapK that will still be effective for us.  As a prior chemo user, i realize that if i had this info. sooner, my mel wouldn't have gotten out of control.  WE ARE OUR OWN ADVOCATES...Most ONCS can't keep up with all these new is VITAL that we get educated on our own.
I got this info from the Skin Cancer Foundations website:


Paul­ B.­ Chapman,­ MD­

Attending Physician Melanoma/Sarcoma Service
Memorial Sloan-Kettering Cancer Center Professor of Medicine
Weill Cornell University Medical College New York City

The overall median survival for patients with stage IV melanoma is less than a year, with approximately 10 percent long-term survivors. Although patients can respond to chemotherapy, it has not been possible to show that it improves median overall survival. High-dose interleukin-2 (IL2), an FDA- approved treatment for stage IV, can induce long-term responses in a small percentage of patients (<10 percent) but is highly toxic and difficult to administer. The discovery in 2002 that about half of melanomas harbor an activating mutation in the BRAF gene1 provided a novel target for therapy which has led, in a relatively short period of time, to a new treatment paradigm for metastatic melanoma.

One of the primary evolutionary problems a eukaryotic cell had to overcome was how to transmit extra-cellular signals from the cell surface to the nucleus. One of the primary path- ways that evolved was the MAP kinase (MAPK) pathway (Figure 1a). When a ligand binds to the appropriate receptor tyrosine kinase, a conformational change is induced that leads to the phosphorylation and activation of Ras (H, N, and K). Activated Ras induces the dimerization of the Raf kinases (A, B, and C) as well as their phosphorylation. These activated dimers phosphorylate MEK, which phosphorylates ERK. Activated ERK enters the nucleus and acts as a transcription factor, turning on the transcription of several genes that lead to cellular proliferation and survival. There is also a complicated negative feedback mechanism that keeps this system under control.

Approximately 50 percent of melanomas harbor an activating mutation in the BRAF gene that leads to an activating mutation of the valine at position 600, usually to glutamic acid (V600E) but sometimes to arginine or lysine. In these cells, the MAPK pathway is constitutively activated, being driven by this mutated BRAF kinase. These cells do not have activated Ras, so the Raf kinases are not dimerized. This is an important mechanism for the specificity of BRAF inhibitors.

Vemurafenib (also known as PLX4032), binds to the ATP-binding site of mutated BRAF and locks it into an active conformation, but without ATP, the mutated BRAF cannot phosphorylate downstream MEK and the MAPK pathway is turned off.

However, vemurafenib can also bind to CRAF and to a lesser degree, wild- type BRAF.2 In the wild-type cell, the Raf kinases are dimerized, and when vemurafenib binds to wild-type CRAF or BRAF, this conformational change induces a conformational change in the other member of the dimer pair resulting in transactivation and increased MAPK pathway activity.3 Thus, the specificity of vemurafenib comes from the fact that in cells with BRAF mutations, the cell is driven by activated BRAF, which exists primarily as monomers and is inhibited by the drug (Figure 1b). This model is supported by data from several in vitro studies.





FIGURE 1a. The Mitogen-Activated Protein Kinase (MAPK) Pathway

When bound by their ligand, various receptor tyrosine kinases lead to ERK activation, which triggers cell proliferation and anti-apoptotic pathways. ERK also activates DUSP (dual-specificity phosphatases) and Sprouty, which negatively feed back on ERK and RAS, respectively. In melanomas with BRAFV600E mutations, the MAPK pathway is activated from the level of RAF.  Adapted from Pratilas and Solit, Clin Cancer Res 2010; 16:3329, with permission.



The first human phase I trial with vemurafenib (then designated PLX4032) began in 2006. Early on in the study, at the lower dose levels, it became clear that the drug could induce dramatic responses in melanoma tumors harboring a V600E mutation4 (Figure 2). The maximum tolerated dose (and the recommended phase II dose) was deter- mined to be 960 mg po bid. An extension cohort of 32 melanoma patients with V600E mutations treated at this recommended phase II dose showed that most patients experienced tumor shrinkage and that 56 percent qualified as having a partial or complete response by RECIST [Response Evaluation Criteria in Solid Tumors] criteria. At 2 years, 7 of 22 patients were still on the study drug.

Recently, the results of a phase II trial (termed BRIM2) were reported.5 In this multicenter trial, 132 melanoma patients harboring a BRAFV600E mutation who had disease progression after at least one prior therapy were treated with vemurafenib at 960 mg po bid. In this trial, in which the tumor responses were reviewed by a central, independent panel, the response rate by RECIST criteria was 52 percent, consistent with the phase I experience. The median overall survival had not been reached at 12 months, indicating that responses can be durable.

In the two studies, the toxicities seen were similar. Arthralgias and fatigue were the most common dose- limiting toxicities. Other common toxicities were alopecia, rash, palmar- plantar dysesthesia, and photosensitivity. Although these were generally grade I or II in severity, occasionally they were grade III.

Drugs that inhibit Raf kinases are known to induce non-melanoma skin tumors. Consistent with this, ap- proximately 25 percent of patients on vemurafenib developed skin tumors characterized as verrucae, keratoacanthoma, or squamous cell carcinoma. These tumors were simply excised. There were no instances of meta- static cancers (other than melanoma) or squamous cell carcinoma in other anatomical sites beyond the skin.

This high response rate justified conducting a phase III trial in which stage IV (or unresectable stage III) previously untreated melanoma patients whose tumor harbored a BRAFV600E mutation were randomized 1:1 to either vemurafenib at 960 mg po bid or standard chemotherapy (dacarbazine 800 mg/ m2 iv every 3 weeks).6 The primary endpoints were overall survival and progression-free survival. Between January and December, 2010, 675 patients were accrued to this trial among 104 participating centers worldwide. In January 2011, the planned interim analysis was performed, at which time the independent data safety monitoring committee announced that the primary endpoints of the trial had been met and recommended that patients randomized to dacarbazine be allowed to cross over to vemurafenib.

Despite the very short follow-up time (median 3 months), the vemurafenib group had a 63 percent lower hazard of death and a 74 percent lower hazard of progression compared to the dacarbazine group (Figure 3). Although median overall survival could not be reliably estimated at this first analysis due to the very short median follow- up, 6-month overall survival rates were 84 percent for the vemurafenib group compared to 64 percent for the dacarbazine group. As expected, the response rate in the vemurafenib patients was much higher (48 percent) compared to the dacarbazine patients (5.5 percent). Progression-free survival, a co- primary endpoint, was also significantly superior on the vemurafenib arm. The median time to progression was 5.3 months compared to 1.6 months with dacarbazine.

Based on these data, and supporting data from the phase II trial, the FDA approved vemurafenib (trade name ZelborafTM) for the treatment of meta- static melanoma harboring a BRAFV600E mutation on August 17, 2011.





FIGURE 1b. Activity of RAF Kinase

In a quiescent, wild-type cell, RAF exists as monomers with only a limited ability to activate MEK (1). When upstream RAS is activated (typically as a result of a ligand binding to a receptor tyrosine kinase), RAF dimerizes, which results in enhanced ability to activate MEK (2). If vemurafenib is added, it binds to the ATP-binding site of one of the RAF molecules, leading to a conformational change that inactivates that molecule but further activates the associated RAF molecule (transactivation) (3). This leads to a further enhancement of MEK activation. If excess drug is added, both RAF molecules can be blocked, leading to shutdown of the pathway (4). However, it is thought that the concentration needed to achieve this is beyond the maximal tolerated dose in humans. In a cell with a BRAFV600E mutation, there is no upstream RAS activation, so the RAF molecules are not dimerized (5). The mutation is sufficient to drive the pathway. However, if vemurafenib is added, the monomers are inhibited, and since there is no dimerization, transactivation does not occur (6). From Poulikakos and Rosen, Cancer Cell 2011; 19:11, with permission.





The clinical trials with vemurafenib consistently show a median time to progression of 5-7 months. This indicates that melanomas can develop resistance to vemurafenib relatively quickly. Therefore, it is critical to understand the mechanism of resistance.

The experience with inhibiting mutated KIT in GIST (gastrointestinal stromal tumors) using imatinib predicted that melanomas developing resistance to vemurafenib would develop a second mutation in BRAF that would prevent binding of the drug. This has not been the case. In some cases of resistance, however, the tumor has developed an activating mutation in upstream NRAS which reactivates the MAPK pathway. Recently, Poulikakos and colleagues have reported a novel resistance mechanism in which a splice variant in the mutated BRAF allele results in the loss of a domain that prevents dimerization.7 As a result, the truncated BRAFV600E kinase readily dimerizes with other RAF kinases despite the lack of upstream RAS activation. By the trans- activation mechanism described above (Figure 1b), these dimers now activate the MAPK pathway in the presence of the drug and result in resistance. Other investigators have described potential resistance mechanisms that can reactivate the MAPK pathway through down- stream events, or mechanisms that activate the parallel PI3K [phosphatidylinositol 3-kinases] pathway.8-10 It re- mains to be determined how frequently these mechanisms play a role in patients developing resistance to vemurafenib. It is likely that other mechanisms re- activating the MAPK pathway will be described in these patients.





FIGURE 2. FDG-PET scans in a patient with metastatic BRAFV600E mutated melanoma treated with vemurafenib

Pre-treatment (A), there is obvious metastatic disease in the lungs and right axillary lymph nodes. After 15 days of therapy (B), FDG uptake has been almost entirely blocked. From Flaherty KT, et al. N Engl J Med 2010; 363:809-19, with permission.






Vemurafenib was FDA-approved for use in metastatic melanoma just 9 years after the first report that melanomas often harbor BRAFV600E mutations. This represents a remarkable amount of collaborative work among those in the melanoma community and the pharmaceutical industry. Other BRAF inhibitors are also in development, most notably GSK2118436, which has recently completed a phase III trial. In this study, 200 patients were randomized 3:1 to GSK2118436 vs. dacarbazine, the primary endpoint being progression-free survival. Results are expected in 2012.

Although 90 percent of BRAF mutations are V600E, about 5 percent are V600K; other mutations make up the remaining 5 percent. In the phase II and phase III vemurafenib trials, a small number of patients were found retrospectively to have had a V600K mutation. Forty percent of these patients responded, indicating that melanomas with V600K mutations are also sensitive to vemurafenib. In the future, it will be necessary to test the other less frequent, non-V600E mutations.















FIGURE 3. Kaplan-Meier plot of progression-free survival (A) and overall survival (B) in the phase III trial of vemurafenib vs. dacarbazine as first-line therapy in patients with metastatic BRAFV600E mutated melanoma

Data represent the planned interim analysis, at which time the median follow-up was 3 months. Tick marks represent censored patients. The number of patients evaluable after 7 months was too low to provide reliable estimates in either treatment arm. From Chapman PB et al. N Engl J Med 2011; 364:2507-16, with permission.





The efficacy of BRAF inhibitors on brain metastases is currently un- clear. Despite the fact that neither GSK2118436 nor vemurafenib were predicted to cross the blood-brain bar-ier, the phase I trial of GSK2118436 gave encouraging results. Of 10 patients treated with brain metastases, 8 showed shrinkage of  > 30 percent and several had complete responses in the brain. A formal phase II trial in patients with brain metastases has recently completed accrual with GSK2118436 and another is under way with vemurafenib.

The infrequency of complete responses with vemurafenib and the frequency with which melanomas develop resistance suggest that combination therapies will be needed. There are currently ongoing trials adding MEK inhibitors, ipilimumab (YervoyTM), or bevacizumab to BRAF inhibitors.

Other rational combinations are also under consideration. [See “Combining Forces: Vemurafenib and Ipilimumab To Be Tried Together."]

  1. Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature 2002; 417:949-54.
  2.  Bollag G, Hirth P, Tsai J, et al. Clinical efficacy of RAF inhibitor needs broad target blockade in BRAF-mutant melanoma. Nature 2010; 467:596-9.
  3. Poulikakos PI, Zhang C, Bollag G, Shokat KM, Rosen N. RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF. Nature 2010; 464:427-30.
  4. Flaherty KT, Puzanov I, Kim KB, et al. Inhibition of mutated, activated BRAF in metastatic mela- noma. N Engl J Med 2010; 363:809-19.
  5. Ribas A, Kim KB, Schuchter LM, et al. BRIM-2: An open-label, multicenter phase II study of RG7204 (PLX4032) in previously treated patients with BRAFV600E mutation-positive melanoma. In: American Society of Clinical Oncology; 2011 June 4, 2011; Chicago; 2011.
  6. Chapman PB, Hauschild A, Robert C, et al. Im- proved survival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med 2011; 364:2507-16.
  7. Poulikakos PI, et al. Nature 2011 (in press).
  8. Johannessen CM, Boehm JS, Kim SY, et al. COT drives resistance to RAF inhibition through MAP kinase pathway reactivation. Nature 2010; 468:968-72.
  9. Nazarian R, Shi H, Wang Q, et al. Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. Nature 2010; 468:973-7.
  10. Villanueva J, Vultur A, Lee JT, et al. Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K. Cancer Cell 2010; 18:683-95.


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boot2aboot's picture
Replies 3
Last reply 2/25/2012 - 8:12pm

After having an excruciating 9 hour proceedure done to get rid of squamous cell cancer andcosmetic reconstruction, i came across an article that may be of some importance for zelboraf users....


Roche’s Zelboraf for Melanoma Spurs Other Skin Cancer’s Growth, Study Says
By Naomi Kresge - Jan 18, 2012 5:00 PM ET

Roche Holding AG (ROG)’s melanoma drug Zelboraf speeds growth of another type of skin cancer, researchers said today in a study underscoring the need to test the medicine in combination with a second treatment.

Scientists at the Institute of Cancer Research analyzed DNA in 21 tissue samples from Zelboraf patients who developed cutaneous squamous-cell carcinoma. About 60 percent of the samples had one of two known cancer-causing gene mutations not targeted by the drug, they said in an article published in the New England Journal of Medicine today.

About 15 percent to 30 percent of melanoma patients treated with Zelboraf and other so-called BRAF inhibitors develop non- melanoma skin cancers, the researchers said. The drugs speeds squamous-cell carcinoma in patients who would probably have gotten the cancer anyway, they said.

“It’s acting as an accelerator of the inevitable in patients that are already predisposed to the disease,” said Richard Marais, a professor of molecular oncology at the London- based institute.

Combining Zelboraf with a second type of drug may stem the effect, said Marais, a co-author of the study, in a telephone interview. Using a type of medicine known as a MEK inhibitor to attack the same pathway that stimulates cell growth appeared to block development of the second type of tumor in mice, the researchers said.

Roche began testing Zelboraf, which works by blocking a protein that fuels tumor growth in about half of patients with advanced forms of melanoma, together with a MEK inhibitor known as GDC-0973 in the BRIM7 patient trial last year. The Basel, Switzerland-based drugmaker helped sponsor the institute’s research.

U.S. regulators approved Zelboraf for sale in August. The European Medicines Agencyrecommended the drug be approved last month. Roche is awaiting a final decision from the European Commission.

To contact the reporter on this story: Naomi Kresge in London at

To contact the editor responsible for this story: Phil Serafino at

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Carole K's picture
Replies 14
Last reply 2/29/2012 - 4:56am

HI Everyone,

I frequented this board from 1999 until around 2008 and certainly do miss all my old frends from MPIP.  I knew so many people here, we got together in ASheville NC< MIchigan, Florida, Seattle, Vancouver and on and on.  They were good times and sad times . Most importantly the support I got here could never be measured. I will all cherish everyone here  and all the love we gave each other. 

For all of you I just want to say DO NOT GIVE UP.  NEVER GIVE UP HOPE.  I should have been dead 11 years ago and I am still kicking. Doing well, getting a bit old these days and loving life. 

I was dx in 1995 with ulcerated mole on my back as a stage II.  Fast forward to 2001 when dx with lung mets and in Dec. 2001 with a brain met.  It was not an easy journey and yet it could have been far more difficult had it not been for this board.  The support I got here cannot be measured.  There was alwasy HOPE>  We would often spend all night in the chat room and let me assure you , if you were depressed when you went in, you were laughing long before you left. 

The one thing my oncologist told me I have never forgotten..CAROLE, DO NO LOOK AT STATISTICS.. NOONE CAN TELL YOU HOW THEY WERE ARRIVED AT.  FURTHERMORE YOU ARE AN INDICIDUAL AND EVERYONE IS  " DIFFERENT".  I hung on to those words for dear life and here I am 11 years later having the best affair with NED, the only man I have never minded sharing.......even with men. 


Sending positive thoughts to all of you




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