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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arthurjedi007's picture
Replies 4
Last reply 1/1/2014 - 7:34am
Replies by: Anonymous, buffcody, arthurjedi007, ecc26

Got my blood work today before my 3rd dose of ipi(yervoy). Anyone know what a large increase means in eosinophils? 3 weeks ago it was 2.7 with an absolute of .2. Today it is 8.0 with an absolute of .5.

I was also wondering if ipi is working should we also see an increase in our absolute lymphocytes? 3 weeks ago mine was 1.2 and now it is 1.1 so really no change.

Typically my numbers are closely the same so to see a number more than double is odd and has me wondering what's happening. I assume it is a reaction to ipi so that is great but I dunno. My dr did not mention anything about it just said my blood work looks good.

Thanks everyone and I hope the new year is great for all of us mel warriors.

 

 

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mitchwendy's picture
Replies 2
Last reply 12/31/2013 - 10:40am
Replies by: mitchwendy, sbrooks90

If you had this done, how long did you wait before returning to exercise, specifically running?
 

They say "return to normal activities", but would that include running? I had 5 nodes removed (all free! ) and I did do 20 minutes with walk breaks yesterday and did not have any new swelling or increased pain....

Just curious as to what others experiences were....

 

Thanks!

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Brendan's picture
Replies 3
Last reply 1/1/2014 - 9:09am
Replies by: ReginaTink, Anonymous, POW

Hi Everyone,

I hope the holidays are treating you well.  

I am happy to report that I am now in a PD-1 trial.  I am receiving nivolumab every other Friday for at least five more doses. If I respond then I will receive six additional doses.  The clinical trial is in Tampa and I live in Philadelphia.  I have flown down twice and the bills are already adding up.  USAir and Southwest fly daily and I am going to look into their medical travel programs.

Does anyone know of any agencies, non-profits, etc., that help cancer patients with travel expenses?  The primary expense is obviously airfare, but car rental adds up too.

Thanks and good luck to you,

Brendan

 

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PracticeUpdate: In your view, which development that occurred in 2013 in melanoma research could have the most significant impact on clinical practice?

Dr. Kirshner: The reporting of the results of additional clinical trials of antibodies against the programmed death 1 (PD-1) receptor and ligand (PD-L1).

The most striking of these studies was presented at ASCO 2013 and promptly published by Wolchok et al in The New England Journal of Medicine in July.1 Metastatic melanoma patients treated with the combination of ipilimumab and nivolumab had a disease control rate of over 65%! The majority of responses were major and are predicted to be durable.

Additional reports of T-cell checkpoint inhibition presented at ASCO add to the growing body of evidence that inhibitors of CTLA-4, PD-1, and PD-L1 are effective treatments for melanoma, with a number of long-term survivors. Patients progressing on ipilimumab can respond to nivolumab or even to retreatment with the same drug and schedule.

PracticeUpdate: What specific changes have you observed or do you foresee as a result of this development?

Dr. Kirshner: I expect FDA approval of nivolumab in the next year and the approval of even more checkpoint inhibitors in the near future.

PracticeUpdate: Would you put this development into historical perspective for the practicing physician?

Dr. Kirshner: Not too long ago, treatment options for metastatic melanoma were very limited. Responses to chemotherapy are poor, in general, and toxicity can be substantial. Immunotherapy (interferon and IL-2) is toxic, for the most part, but occasional durable responses were seen, usually in patients with more limited disease.

T-cell checkpoint inhibitors have a different mode of action than prior treatments (blocking inhibition activates T cells for more effective immune destruction of the metastases). These are the most active treatments for metastatic melanoma to date, and toxicities are manageable.

PracticeUpdate: Would you sum up in a single sentence why you chose this development as the top story of the past year?

Dr. Kirshner: The development of new T-cell checkpoint inhibitors (specifically anti-PD-1 and anti-PD-L1) not only adds to the armamentarium of treatments for advanced melanoma, but there are reasons to believe that these drugs will be active in a wide range of malignancies that would respond to immunotherapy.

Reference

  1. Wolchok JD, Kluger H, Callahan MK, et al. Nivolumab plus ipilimumab in advanced melanoma. N Engl J Med. 2013;369(2):122-133.

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lll.ll.lll.ll.lll's picture
Replies 7
Last reply 1/4/2014 - 12:01am

I'm so glad I have found this.. I've been a little lost with all this and seems that nobody really wants to talk about it so I'm hoping I can find some input here.

I started noticing something was wrong back in late Aug early September.. I was tired all the time. I'm physically active and workout five to six days a week and was doing a very physical job at the time but I was really the only one struggling dieting it physically with being so tired.

It was during that time I started to notice a swimy feeling in my head and I was getting confused and angry at almost nothing. I honestly thought I was getting early dementia or had cte.

Two months later I was still tired and having the same issues with my brain.. I would describe it as taking pain killers on an empty stomach and the sick feelings that come with. But I kept brushing it off till one morning I woke with a severe burning feeling on a spot on my back. When I went to look in the mirror it was a dark spot I had had for years and apon touching it it began to ooze dark thick blood.

Being uninsured two days later I found a dermatologist that would perform the biopsy. I told the nurse and the Dr what I had been going through. The Dr only visually looked at my back and said there were a few spots he was concerned about but the one I came in for definitely needed to be biopsied.

A week later the results came back that it was in fact melanoma and it needed to be removed and he recommend I get health insurance to get it taken care of.

Well my insurance wont kick in till the first of the year and other things keep popping up.. I still have the swimy brain only worse now.. I stumble now sometimes when I walk.. I've noticed lymph nodes in my pelvis get larger over the past month or so and now I'm getting pains in the area.. I get a stabbing pain in my diaphragm from time to time and I find it hard to catch my breath..

I've been to the er twice now cause it gets so bad..

My white count is "elevated" and they say it can be from just an infection.. my brain scan had some admoralities but nothing "acute" and my chest xray looked "alright"

I know er and Dr talk all to well and they dance around things.. I guess I'm hoping maybe someone has had similar symptoms

Adam McCurry

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hdelancey23's picture
Replies 10
Last reply 12/30/2013 - 11:23pm

I am up visiting my mom for Christmas. And it has been a great time. My mom is doing as well as can be expected. The morphine is really helping in managing her pain at home. She does okay through the day but it is the mornings that are the worst on her. It is hard for her to get up out of bed and very painful for her. I guess it is from the morphine wearing off through the night and it seems like her body is very very stiff. She has consultation for WBR next week and will start next week as well. I am nervous to see how she takes a second dose of it. I am just praying that it might buy some more time to get into the pd1 trials. At this point for me any more Tim that we can get is very precious. She is such a fighter and so strong. Her doctors told her last December that she only had three to six months and now here we are a year later. To all those that are fighting this horrible disease and to family members that are watching their loved ones struggle you can't always go by what the doctors say. Keep fighting and keep hoping.

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Bob B.'s picture
Replies 3
Last reply 1/9/2014 - 11:25am
Replies by: lsmith - MRF, Anonymous, BrianP

it's been awhile since I visited.   The site has changed.

 

How do I "search" a previous Topic?

 

Thanks!

 

Bob B.

The Only Good Legend is a Dead Legend.

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Janet Lee's picture
Replies 5
Last reply 1/13/2014 - 11:19am

I've seen a couple of posts recently about left-over melanoma drugs, as well as cautionary replies about scams, confidentiality, etc. I think this is a very valid topic, and would like to know if there are any "legitimate" ways to donate any of these expensive drugs to the melanoma patients who may be without insurance or are being denied the medicine for whatever reason.

Seems to me there should or could be some sort of clearing house to help others?

Janet Lee

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JerryfromFauq's picture
Replies 10
Last reply 1/1/2014 - 3:56am
Replies by: JerryfromFauq, Joannezaras, POW, Anonymous, JoshF

Tried to post the URL so that you could read the whole long article.  Here's the start.    This is in response to the Gal that has been telling people that one must kill their immunsystem before they can receive IL-2. 

2013 IL-2 & T-Regs   Does IL-2 require killinig Immune system (Which includes our T-cells)?
Introduction

High-dose (HD) bolus IL-2 therapy is currently one of the most potent forms of immunotherapy and was approved by the FDA as a single-agent cytokine therapy for metastatic melanoma and renal cell carcinoma (1–3). Typical HD IL-2 therapy consists of bolus infusions of 600,000 or 720,000 IU/kg of aldesleukin (Novartis), and each cycle of therapy is aimed at giving up to 15 bolus infusions every 8 hours or as many as the patient can withstand due to toxicity (1, 4). The therapy cycle is then repeated approximately every 14 to 21 days for up to 6 to 8 cycles, depending on the clinical performance of each patient and toxicities associated with IL-2 therapy. Early single and multicenter clinical trials have consistently shown a 15%–16% partial and complete response rate in patients with stage IIIC or stage IV noncutaneous metastatic melanoma and in patients with renal cell carcinoma, among whom a smaller fraction of patients (about 5%) experience durable long-lasting complete remission for years (1, 2, 5). HD IL-2 has also been combined with other immunotherapies, including adoptive T cell therapy using ex vivo–expanded tumor-infiltrating lymphocytes (6–8) and tumor antigen peptide vaccines (9), where it may enhance antitumor T cell function. IL-2 is known to induce NK cell and CD8+ T cell proliferation, survival, and acquisition of effector function through STAT5 activation (10–12). Increased tumor-infiltrating and circulating perforin+ (PRF1+) NK cells and activated CD8+ T cells have been found in most patients undergoing HD IL-2 therapy, but this finding did not always correlate with tumor regression or clinical response (13–15).

One of the key problems with HD IL-2 therapy, which limits its more widespread use, is its adverse effects, including blood pressure changes, vascular leak syndrome, liver dysfunction, neurological changes (cognitive impairment), and high fever (1, 2). These toxic effects require some patients to withdraw from therapy after a limited number of therapy cycles. Nevertheless, HD IL-2 continues to be a treatment of choice for qualified patients, especially for those with metastatic melanoma, because it is one of the only therapies capable of inducing documented durable clinical remission lasting for many years. Thus, specific biomarkers that can identify subsets of patients who are responsive to HD IL-2, and thereby improve patient selection, are needed to refine this form of therapy and make it more attractive to more clinical centers.

Recently, a number of groups have reported that HD IL-2 markedly expands the classic Treg pool, consisting of CD4+CD25+Foxp3+ Tregs (16–19). Some of these studies have attempted to correlate the extent of Treg expansion during IL-2 therapy with clinical outcome and have suggested a negative correlation between a sustained increase in Tregs during multiple IL-2 therapy cycles and progressive disease (17). Tregs inhibit effector CD8+ and CD4+ T cells by suppressing their proliferation or inducing cell death. Moreover, Tregs can also antagonize NK cell–mediated antitumor activity (20–23). However, the exact role of Tregs in HD IL-2 therapy needs to be further defined.

Tregs exist in two main forms: the so-called natural Tregs, originally derived from the thymus, and induced Tregs, generated from peripheral naive CD4+ T cells in the presence of TGF-β and IL-2 (22, 24, 25). However, the phenotypic markers distinguishing these two main Treg types are still unclear. Although previous studies have tracked the appearance of Tregs during IL-2 therapy by using the classic markers CD25, Foxp3, cytotoxic T lymphocyte antigen 4 (CTLA4), glucocorticoid-induced tumor necrosis factor receptor (GITR), and CD127, Tregs may exist in various states of differentiation and activation that may be discernible with use of additional markers. For example, a subset of Tregs may be tumor antigen specific and activated through the TCR before HD IL-2 therapy; these cells may carry specific activation markers reflecting this ongoing antigenic stimulation that clearly separates them from the bulk circulating Treg population. Thus, these previously “activated” tumor-specific Tregs may be induced to further divide by IL-2 treatment.

In this article, we investigated which lymphoid and myeloid subsets were modulated upon HD IL-2 therapy and their possible association with clinical response to allow preidentification of patients who can benefit from this treatment. We performed comprehensive multiparameter flow cytometry analysis to determine the changes in more than 40 different lymphocyte subsets, including subpopulations of Tregs, DCs, and CD4+, CD8+, NK, and B cells in PBMCs from patients treated with HD IL-2 before IL-2 infusion and 2 days after the last infusion of cycle 1 of HD IL-2 therapy. After analyzing the fold changes of each cell subset, we found that CD4+ICOS+ T cell subset, consisting almost exclusively of CD25hi and Foxp3hi Tregs (ICOS+ Tregs), was one of the most rapidly expanding lymphocyte subsets in response to IL-2. We present data characterizing the phenotype of CD4+ICOS+ and ICOS+ Treg subsets during the first cycle of HD IL-2 therapy and their potential as predictive biomarkers.
Results

Activated T cells within a CD4+ICOS+ subset greatly increase during IL-2 therapy. We developed a multicolor FACS staining panel to track changes in multiple lymphocyte subsets in peripheral blood of patients with melanoma during cycle 1 of HD IL-2 therapy. This panel allowed us to track the changes in multiple T cell, B cell, DC, and NK cell lineages before and after HD IL-2 therapy. First, we analyzed the first 9 patients consecutively treated with HD IL-2 (Supplemental Table 1; supplemental material available online with this article; doi: 10.1172/JCI46266DS1). Blood was collected immediately before the first bolus infusion of IL-2 and during the rebound period, which is 2 days after the last IL-2 infusion, when a rapid influx of lymphocytes back into the blood occurs (16, 26, 27). This sample 2 days after IL-2 treatment gives us a “window” into the immediate changes that are induced in patients during the first cycle of IL-2 therapy. A heat diagram of the FACS data shows the fold change in 46 lymphocyte subsets as a percentage of total live lymphocytes (Figure 1A). Strikingly, although minor changes occurred in a number of lymphocyte subsets, some major cell types consistently exhibited markedly high increases in all patients during IL-2 therapy, as indicated by the bright red regions in Figure 1A. One of these cell types was the CD4+ T cells, which consisted of ICOS+, CD25+ICOS+, and CD4+CD25+ICOS+ T cells that coexpressed Foxp3 (Figure 1A).
CD4+ T cells expressing ICOS with phenotypic characteristics of Tregs increFigure 1

CD4+ T cells expressing ICOS with phenotypic characteristics of Tregs increase the most in peripheral blood after HD IL-2 therapy. PBMCs isolated at baseline and 2 days after the last dose of IL-2 during cycle 1 of HD IL-2 therapy from 9 patients (nonresponders) were stained for multiple T, B, and NK cell and DC markers. The percentage of 46 cell subsets in the live lymphocyte gate were determined, and the fold change in the frequency of each indicated cell subset in the lymphocyte gate was calculated by dividing the frequency of cells before HD IL-2 therapy by the frequency after treatment. (A) Changes in the percentage of indicated cell subsets analyzed for all 9 patients (patient numbers are shown at the top of the heat map) were heat mapped based on the fold changes, with the use of an Excel conditional formatting program, as indicated at the bottom of the figure. The major lymphocyte subpopulations corresponding to the different phenotypic marker subsets (left side) are indicated on the right side of the heat diagram. (B) Total numbers of CD4+ICOS+, CD4+CD25+ICOS+, and CD4+CD25+Foxp3+ICOS+ cells before IL-2 and 2 days after cycle 1 of HD IL-2 therapy (after IL-2) are shown for these 9 patients. Total cell numbers were calculated by multiplying the percentage of each subset in the viable lymphocyte gate by the absolute lymphocyte count. Horizontal bars represent median values. Statistical analyses were performed with 2-tailed Wilcoxon matched paired test.

The second major cell type that showed a high increase in all patients was NK cells, with a predominantly CD56hiCD16loPRF1+ NK phenotype (Figure 1A) and more than an 80-fold increase in these cells in some patients (median, 25-fold increase; n = 9). Expansion of NK cells and acute sensitivity of these cells to IL-2, as these cells constitutively express CD25 (IL-2Rα), as well as perforin-induced expression by IL-2 were expected on the basis of previous studies on IL-2–treated patients (28–31). All other lymphocyte subsets exhibited either small increases after IL-2 therapy (less than 2 fold) or a decrease, as shown by the blue regions in Figure 1A. Increased frequency of CD11c+ DCs was seen in some patients (median, 3.6 fold), whereas the frequency of CD19+ B cells consistently decreased after IL-2 therapy by 3 fold to 4 fold.

The CD4+ICOS+ and CD4+CD25+ICOS+ cell subsets increased by a median of 13 fold and 27 fold, respectively. However, the most consistent and highest increase was in the frequency of CD4+CD25+Foxp3+ICOS+ T cells (median, 37 fold). We calculated the change in total number of ICOS+ cells in the CD4+ subset by multiplying the absolute lymphocyte counts per milliliter of blood by the percentage of each subset in the live lymphocyte gate. As shown in Figure 1B, the total number of CD4+ICOS+, CD4+CD25+ICOS+, and CD4+CD25+Foxp3+ICOS+ T cells increased greatly after HD IL-2 therapy. Similar results were seen with the .     . http://www.jci.org/

 

I'm me, not a statistic. Praying to not be one for years yet.

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Patina's picture
Replies 8
Last reply 12/31/2013 - 2:06am

Hi,

Does anyone here know or have they experinced a reduction in visible tumors within weeks of taking Yervoy?  I can't find anything on this and wonder if anyone knows how good a sign this might be or not...

My Mother was diagnosed with stage IV and later brain mets.  She had gamma knife radiation for lesions on her brain and 4 days later had her first infusion of Yervoy. 

She had a very large tumor on her neck and 18 small to large tumors on her scalp.  There were 8 small lesions on her brain.

Two weeks later the tumor on her neck has shrunk by 50% and the tumors on her head are now hard compared to what they had been.  She still have 3 more treatments of Yervoy and I'm wondering how positive this might be or not...  

She goes in 3 weeks to get a MRI of her brain and we might know what is happening with her scalp, but its encouraging that the tumor on her neck is much smaller.

 

 

 

 

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Michelem's picture
Replies 11
Last reply 1/2/2014 - 3:58pm
Replies by: JerryfromFauq, kylez, Michelem, arthurjedi007, SABKLYN, Anonymous

My husband had surgery in October -removal of melanoma on the bottom of his foot, and 8 lymph nodes in the groin area. Subsequently another melanoma appeared near the first, and was removed in an in-office procedure.

As he healed, we began screening for the interferon-ipi randomized trial. But that PET scan, just 90 days after the first, showed cancer has now spread to more lymph nodes. This kicks us from the trial - so disappointing. In two weeks he will have surgery to remove more lymph nodes. We are told a two-hour procedure and at least one night hospital stay. So it seems like a serious procedure. 

What next? Does anyone know what this quick recurrence means in terms of possible further spread? I assume we may get back in line for the randomized trial once he is healed from this surgery. Based on previously experience, that is likely to be at least a couple of months - which seems like a long time to wait. 

Thanks so much for insights, thoughts . . . . and prayers!  mm

MicheleM

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Jahendry12's picture
Replies 6
Last reply 12/27/2013 - 11:13pm

I have been reading entries on this bulletin board all day today.  It's nice to know I am not alone in this fight. My husband was diagnosed with nodular melanoma in April 2011. After 2 surgeries and a SNB, they also found he had a rare lymphoma. My husband is a healthy, active man that has been, & remains asymptotic. Since he was diagnosed, he has had  5 surgeries, no treatments. He had a lung nodule removed in march of this year & we have CT's every 3 months - so far so good.

As you all know, this a nightmare roller coaster ride that you just want to wake up from.  I don't talk about it a lot because I find that it's hard for people to understand what we are going through.  I appreciate everyone's openness & honesty on this site. I finally found people that live what I live, feel what I feel, & have the same questions, concerns & worries that I am experiencing.   God bless & I pray for you all

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Anonymous's picture
Anonymous
Replies 4
Last reply 1/2/2014 - 5:11pm
Replies by: JerryfromFauq, Anonymous, casagrayson

The counts went crazy, so that feature was apparently removed.  Now we are speaking to a blank wall. 

Couldn't we have this feature fixed?  It gives a sense of community to know people are out there.  Otherwise, there are only a few replies, or none at all and you wonder: Is anyone there?  Without these counts, who knows?

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Anonymous's picture
Anonymous
Replies 3
Last reply 12/27/2013 - 11:50am
Replies by: NYKaren, POW
Salvage Radiosurgery for Brain Metastases: Prognostic Factors to Consider in Patient Selection
Int. J. Radiat. Oncol. Biol. Phys 2014 Jan 01;88(1)137-142, G Kurtz, G Zadeh, G Gingras-Hill, B-A Millar, NJ Laperriere, M Bernstein, H Jiang, C Ménard, C Chung
Research · December 19, 2013
 
 

TAKE-HOME MESSAGE

  • "Among patients who have received stereotactic radiotherapy for recurrent brain metastases after prior brain radiation therapy, factors predicting for improved overall survival were younger age, extracranial disease control, and interval time from initial radiotherapy to salvage of at least 265 days."

- Chris Tully, MD

  • This study highlights the possibility of durable responses in patients with recurrent brain metastases treated with salvage SRS.

ABSTRACT

Purpose

Stereotactic radiosurgery (SRS) is offered to patients for recurrent brain metastases after prior brain radiation therapy (RT), but few studies have evaluated the efficacy of salvage SRS or factors to consider in selecting patients for this treatment. This study reports overall survival (OS), intracranial progression-free survival (PFS), and local control (LC) after salvage SRS, and factors associated with outcomes.

Methods and Materials

This is a retrospective review of patients treated from 2009 to 2011 with salvage SRS after prior brain RT for brain metastases. Survival from salvage SRS and from initial brain metastases diagnosis (IBMD) was calculated. Univariate and multivariable (MVA) analyses included age, performance status, recursive partitioning analysis (RPA) class, extracranial disease control, and time from initial RT to salvage SRS.

Results

There were 106 patients included in the analysis with a median age of 56.9 years (range 32.5-82 years). A median of 2 metastases were treated per patient (range, 1-12) with a median dose of 21 Gy (range, 12-24) prescribed to the 50% isodose. With a median follow-up of 10.5 months (range, 0.1-68.2), LC was 82.8%, 60.1%, and 46.8% at 6 months, 1 year, and 3 years, respectively. Median PFS was 6.2 months (95% confidence interval [CI] = 4.9-7.6). Median OS was 11.7 months (95% CI = 8.1-13) from salvage SRS, and 22.1 months from IBMD (95% CI = 18.4-26.8). On MVA, age (P=.01; hazard ratio [HR] = 1.04; 95% CI = 1.01-1.07), extracranial disease control (P=.004; HR = 0.46; 95% CI = 0.27-0.78), and interval from initial RT to salvage SRS of at least 265 days (P=.001; HR = 2.46; 95% CI = 1.47-4.09) were predictive of OS.

Conclusions

This study demonstrates that patients can have durable local control and survival after salvage SRS for recurrent brain metastases. In particular, younger patients with controlled extracranial disease and a durable response to initial brain RT are likely to benefit from salvage SRS.

International Journal of Radiation Oncology, Biology, Physics
Salvage Radiosurgery for Brain Metastases: Prognostic Factors to Consider in Patient Selection
Int. J. Radiat. Oncol. Biol. Phys 2014 Jan 01;88(1)137-142, G Kurtz, G Zadeh, G Gingras-Hill, B-A Millar, NJ Laperriere, M Bernstein, H Jiang, C Ménard, C Chung

 

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Stage III/IV Melanoma Patients at Risk for New Primary

 

J. Clin. Oncol 2013 Dec 02;[EPub Ahead of Print], L Zimmer, LE Haydu, AM Menzies, RA Scolyer, RF Kefford, JF Thompson, D Schadendorf, GV Long

Research · December 24, 2013
 
 
 

TAKE-HOME MESSAGE

  • This long-term follow-up of > 4000 patients reported a 5.6% rate of second primary melanoma at 10 years in patients with stage III disease at initial diagnosis.
  • Risk of developing a second primary was higher in males and in those with history of multiple melanomas in the past.

- Richard Bambury, MD

 

ABSTRACT

 

PURPOSE

New primary melanomas (NPMs) have developed in some patients with metastatic melanoma treated with BRAF inhibitors. We sought to determine the background incidence of spontaneous NPMs after a diagnosis of American Joint Committee on Cancer/International Union Against Cancer stage III or IV melanoma in patients not treated with a BRAF inhibitor.

 

PATIENTS AND METHODS

Patients diagnosed with stage III or IV melanoma at Melanoma Institute Australia between 1983 and 2008 were analyzed, and those who received a BRAF inhibitor were excluded.

 

RESULTS

Two hundred twenty-nine (5%) of 4,215 patients with stage III melanoma and 43 (1%) of 3,563 patients with stage IV melanoma had at least one NPM after diagnosis of stage III or IV disease. The 6-month, 1-year, and 10-year cumulative incidence rates of developing an NPM after stage III melanoma were 1.2% (95% CI, 0.86% to 1.51%), 1.8% (95% CI, 1.44% to 2.26%), and 5.9% (95% CI, 5.08% to 6.74%), respectively. The 3-month, 6-month, and 1-year cumulative incidence rates of NPM after diagnosis of stage IV melanoma were 0.2% (95% CI, 0.07% to 0.36%), 0.3% (95% CI, 0.15% to 0.51%), and 0.4% (95% CI, 0.25% to 0.7%), respectively. In both patients with stage III and stage IV melanoma, male patients and patients with a prior history of multiple primaries had a higher incidence of NPM.

 

CONCLUSION

Patients with stage III and stage IV melanoma remain at risk for development of further primary melanomas, particularly if they have a history of multiple primary melanomas before stage III or IV disease. The incidence rates are lower than those reported in patients receiving BRAF inhibitors. However, the results must be compared with caution because dermatologic assessment is more frequent in BRAF inhibitor trials.

 

Journal of Clinical Oncology
Incidence of New Primary Melanomas After Diagnosis of Stage III and IV Melanoma
J. Clin. Oncol 2013 Dec 02;[EPub Ahead of Print], L Zimmer, LE Haydu, AM Menzies, RA Scolyer, RF Kefford, JF Thompson, D Schadendorf, GV Long

 

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