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

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Hi everyone - new here! :)   I have a question about "dissolving stitches" <-- only putting quotations around them because they aren't seemingly dissolving.  The stitches on my upper, left back - you can physically feel them through the skin.  You can feel them running from one side to another and it's been almost 4 months.  Surgery date was April 12th and they are defintely still there.  Now, the incision under my left arm is fine; I don't feel any stitches there.  

The only thing different is that obviously the skin on your back is tighter....maybe that is the problem?  It doesn't hurt at all, I'm not having any issues (other than of course the random sharp pains that you feel from the sites - but I wouldn't call that an "issue" per se).  

Has anyone else run into this with "dissolving" stitches?  How long did they typically take to dissolve?  

 

~Amber~

holymolymelanomy.blogspot.com/ 

"Everything happens for a reason"

holymolymelanomy.blogspot.com

 

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Kellie-T's picture
Replies 9
Last reply 8/7/2013 - 6:25pm

All,

I read posts but don't post that much here. Everyone has a story to tell and I'm thankful we have this forum to share because it helps me cope knowing you are out there and can relate to what is going on within all of us. On to my great news.....scans on July 25th (neck to pelvic CT and brain MRI) - "no evidence of metastatic disease present." Also, lab work continues to be very well. The doc put it like this, "18 months on treatment, scans are consistently great (NED) for the past year, much like remission".

I'm always cautious because this disease comes and goes as it pleases. I'm doing my part to stay healthy and enjoy life. I'm thankful for each and every day. The side effects are very tolerable (take six pills per day). My onc says that since I'm tolerating so well and my labs look great she sees no need in taking a break from treatment. Why mess with it when it is working so well?

Just wanted to share my little Z story.

 

Thanks,

Kellie

Life is not by accident. Make every minute count.

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POW's picture
Replies 10
Last reply 8/7/2013 - 5:47pm

I just found out about two clinical trials for Novartis' new BRAF inhibitor LGX818.  LGX818 is a lot like Zelboraf but it binds tighter to the BRAF protein so it might be harder for the tumor to develop resistance. You still have to have the BRAF V600E mutation, though.

Novartis is sponsoring 2 clinical trials-- one of LGX818 alone ( http://clinicaltrials.gov/show/NCT01436656 ) and one of LGX818 + the MEK inhibitor MEK162 ( http://clinicaltrials.gov/show/NCT01543698 ). The number of sites is still small, but new sites will be recuriting soon (including Moffitt).

The best news is that according to Dr. Gibney at Moffitt, LGX818 has been shown to have activity in patients who became resistant to Zelboraf AND  having a history of Zelboraf does not exclude you from this trial!

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VSlim's picture
Replies 9
Last reply 8/7/2013 - 5:42pm

Hi all, This is my first posting on the site. My husband was diagnosed two years ago (unknown origin, it showed up in the lymph nodes in his neck). He has been treated at Sloan Kettering with surgery, radiation, and most recently ipilimumab but the disease is still spreading. His doctor at Sloan is recommending their clinical trial of Bristol Myers' anti PD-1 (nivolumab) but it's randomized v. chemo. I've been searching for a nonrandomized trial of the Merck anti PD-1 in our area (New York) but so far no success. The clinicaltrials.gov site has twice given me hope--only to find that the trials are no longer enrolling. If anyone knows of a trial in our area, I'd very much appreciate knowing about it.

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Hi, I've seen others post their pathology reports here so I am hoping to get some help deciphering my own.  I was just diagnosed today with malignant melanoma in one mole.  I met with my dermatologist who *somewhat* explained the details of my diagnosis but was unable to tell me what stage I am in. She did explain that I will have the surgery to remove the entire mole and "that should take care of it."  I asked her if there was any indication that my cancer had spread or if there will be any follow up treatment.  She said there are no guarantees but "the odds are overwhelmingly in your favor."  I'll continue to have full body scans on a regular basis.  I asked what stage I am in and she sort of shrugged her shoulders and said "stage 1, I guess."  She gave me a copy of my report but did not offer to explain it.  Well, I am trying to focus on her positive attitude and her statement that the odds are overwhelmingly in my favor but would also like some feedback from this forum, if possible.  This is what my pathology report says:

 

"Malignant melanoma measuring 0.3 mm in thickness.

Comment:  There is a broad asymmetrical poorly circumscribed melanocyctic neoplasm composed of nests localized at the dermal epidermal junction and superficial dermis.  There is marked variation in the size and shape of the nests and areas of confluence.  There is no evidence of ulceration or vascular invasion.  The lesion extends to the lateral margins and a conservative reexcision of this lesion to ensure that it is completely removed would be judicious."  

 

I've looked at the stages chart on this site, which leads me to believe I am either Stage 0 or Stage 1A.  Can anyone clarify which one it is?  I've looked up the term ulceration but what exactly does vascular invasion mean?  What is the significance of the statement: "marked variation in the size and shape of the nests and areas of confluence?"  I will be in Mexico July 25-Aug 2 and discussed this with the dermatologist in relation to scheduling of the surgical procedure and recovery with stitches.  I don't want to put off a necessary procedure to remove cancer but I also do not want to be out of the country and have to deal with stitches, in case there are complications.  My dermatologist agreed that I would be better off not having stitches while away and said it should be fine to wait until after I return to have the procedure.  Incidentally, I have developed an infection at this same site from the scraping the doctor did last week for the biopsy and I am now on an antibiotic for the next 10 days.  She said the surgeon would not want to remove the mole until I am infection-free.  Is it safe to wait until early August for the mole removal?

Thank you for your time and advice.    

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Research August 01, 2013
 

 

 

Public Availability of Results of Trials Assessing Cancer Drugs in the United States

 

J. Clin. Oncol. 2013 Jul 22;[EPub Ahead of Print], TA Nguyen, A Dechartres, S Belgherbi, P Ravaud

 

 

 
TAKE-HOME MESSAGE

An analysis of cancer-related clinical trials assessing new drugs with a primary completion date between 2007 and 2010 reveals that almost 50% of trials still had no publicly available results 3 years after completion.

ABSTRACT

Purpose: To evaluate to what extent results of completed trials of cancer drugs conducted in the United States are publicly available at ClinicalTrials.gov, as required by the Food and Drug Administration Amendments Act (FDAAA), or are published in journals.

Methods: We searched ClinicalTrials.gov for cancer trials governed by the FDAAA: phase II to IV trials assessing drugs in the United States with a primary completion date between December 26, 2007, and May 31, 2010. For each trial, we also searched PubMed to identify the publication of results. We assessed the cumulative percentages of posted or published results over time by using the Kaplan-Meier method.ResultsWe identified 646 trials, including 209 randomized controlled trials (RCTs). At 12 months after completion of the trials, the cumulative percentages of trials with results posted at ClinicalTrials .gov, published in journals, and available either at ClinicalTrials.gov or in journals were 9% (95% CI, 7% to 11%), 12% (95% CI, 10% to 15%), and 20% (95% CI, 17% to 23%), respectively, and for RCTs, the percentages were 12% (95% CI, 8% to 16%), 5% (95% CI, 2% to 8%), and 17% (95% CI, 12% to 22%), respectively. At 36 months, these percentages were 31% (95% CI, 28% to 35%), 35% (95% CI, 31% to 39%), and 55% (95% CI, 51% to 59%), respectively, and for RCTs, they were 38% (95% CI, 31% to 45%), 32% (95% CI, 25% to 39%), and 56% (95% CI, 48% to 62%), respectively. Public availability of phase III trials was 15% (95% CI, 7% to 23%) at 12 months, 39% (95% CI, 27% to 49%) at 24 months, and 64% (95% CI, 50% to 73%) at 36 months.

Conclusion: Despite the FDAAA, results for nearly half the trials of cancer drugs in the United States were not publicly available 3 years after completion of the trials.

Journal of Clinical Oncology
Public Availability of Results of Trials Assessing Cancer Drugs in the United States
J. Clin. Oncol. 2013 Jul 22;[EPub Ahead of Print], TA Nguyen, A Dechartres, S Belgherbi, P Ravaud

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Interview August 01, 2013

 

 

Immunotherapy in Melanoma

 

 

 

In this interview, Dr. Michael Postow, Assistant Attending Physician with the Melanoma–Sarcoma Oncology Service at Memorial Sloan-Kettering Cancer Center, and Dr. Tony Nimeh, Research Physician at Brigham and Women’s Hospital, discuss advances in immunotherapy for melanoma.

Dr. Postow is enthusiastic about the promising early data on the effects of blocking the programmed death-1 (PD-1) receptor using nivolumab and lambrolizumab, antibodies with specific activity against PD-1. However, he cautions that therapy using immunomodulators needs to be administered with care because of immune-mediated side effects and the occasional need for immunosuppressants. Large phase III studies will be necessary to determine the full potential benefits of these PD-1 immunomodulatory drugs. The ultimate hope is to win FDA approval for the drugs, making them accessible to the many patients in need.

Dr. Nimeh: Dr. Postow, would you discuss the recent data on nivolumab that were presented at ASCO?

Dr. Postow: Nivolumab is one of several very promising new antibodies that target the PD-1 receptor. Previous data on nivolumab had been published in 2012 in The New England Journal of Medicine1 This year at ASCO, long-term data from those studies were presented, and we learned more about PD-L1 as a potential biomarker for PD-1 therapy with nivolumab.

Dr. Mario Sznol presented long-term data on PD-1 treatment with nivolumab in the Melanoma/Skin Cancers Oral Abstract session.2 The drug toxicity profile was extremely favorable, even over time and with continued dosing. The lack of accumulation of additional toxicities over time is obviously very important with any ongoing, continuous therapy.

The median overall survival also appeared quite favorable, when compared with prior historical data in advanced melanoma. The median overall survival was 16.8 months across all of the different doses that were evaluated. Of course, cross-trial comparisons need to be interpreted with caution, particularly in a phase I trial such as this one; but, these results are certainly promising and, based on the results, several larger-scale, randomized, phase III studies are being conducted to test the drug’s benefits in a larger population.

Potential biomarkers for Nivolumab

Dr. Nimeh: Are there any immunotherapy biomarkers that might help identify the best candidates for nivolumab?

Dr. Postow: At this point, there are no specific biomarkers that have been studied thoroughly enough, and provided data that are convincing enough, to influence the selection of a patient for PD-1 antibody therapy. PD-L1, however, is being examined as a potential biomarker for nivolumab in ongoing large phase III trials.

To put this in context, we need to keep in mind certain principles in immunotherapy. Most anticancer therapies target the tumor itself. With biomarkers, we attempt to detect genetic changes in the tumor, or changes within oncogenic signaling pathways, to help us direct therapies at the tumors. In contrast, all of these immunomodulating antibodies (such as PD-1) act on, and target, the patient’s normal immune cells rather than the tumor itself. Because of that difference, it has been very difficult to identify a biomarker that would influence patient selection. In concept, every patient could potentially benefit from immunotherapy if it was used appropriately and in the right sequence or combination.

There is a lot of discussion about PD-L1 as a potential biomarker for nivolumab and perhaps other PD-L agents. In biomarker studies of PD-L1, patients are considered positive if they have at least 5% membranous staining on the tumor surface by immunohistochemical analysis. These patients preliminarily appear to have a greater likelihood of tumor shrinkage. However, some patients have an excellent response even though their tumors do not have PD-L1 expression. Therefore, patients who do not express PD-L1 should still be considered for treatment with agents such as nivolumab.

Nearly 50% of patients with melanoma have a BRAF mutation. Patients with BRAF mutations are expected to do just as well with nivolumab and other immunotherapies as patients without BRAF mutations. There are no convincing data to suggest that the response to immunotherapy depends on the particular mutation found in the tumor, especially with BRAF. Often, small-molecule targeted therapies, such as vemurafenib, dabrafenib, and trametinib, are approved by the FDA and used for patients with BRAF mutations. Combinations of these targeted agents are also being tested to see if they are better than single agents themselves. 

The specific sequences or combinations of therapies that are most beneficial are still being evaluated in clinical trials.  For a patient who has a mutation such as BRAF, we do not yet know, based on available data, whether it is preferable to start treatment with immunotherapy or with targeted therapy. It has been our practice, for an asymptomatic patient (who does not need an immediate response), to start with immunotherapy. This gives the patient an opportunity for long-term durable benefit. However, for the patient who has symptomatic disease or a large tumor burden, we prefer to begin with targeted therapy, as we feel this gives him or her the best chance for immediate tumor shrinkage (which seems to occur more readily with the targeted agents).

Dr. Nimeh: Blockade of the PD-1 and PD-L1 pathway may be effective against tumors in which PD-L1 is expressed at the cell surface, reflecting a baseline, “preactivated” state of the immune system. Is there anything we can do to up-regulate PD-L1 in cells that are not in such a preactivated state?

Dr. Postow: That’s an excellent question and one that is the focus of several ongoing investigations. It is not yet completely clear which specific treatment modalities would up-regulate PD-L1 because we have not yet done enough prospective trials, with pre- and post-treatment biopsies, to assess PD-L1 changes associated with a specific intervening therapy.

PD-L1 is believed to be up-regulated in the setting of chronic inflammation. This may be a mechanism by which the tumor cells create their own resistance to otherwise effective antitumor immunity. When tumor-infiltrating lymphocytes interact with the tumor, it has been shown (through interferon-gamma secretion) that PD-L1 can be expressed. Thus, perhaps the tumor has found a way to protect itself from these immunologic onslaughts of tumor-infiltrating lymphocytes. Perhaps we need to find ways to increase this immune-cell infiltration within the tumor to cause a PD-L1 up-regulation leading to an increased susceptibility to the beneficial effects of PD-1 therapy.

Bear in mind that we have not yet determined the appropriate sequence or combination to up-regulate PD-L1 clinically, after which we could use the PD-1 antibody to enact a response. It is a critical point that even patients whose tumors are PD-L1 negative can still respond to PD-1 blockade.

Side effects of immunotherapy

Dr. Nimeh: What are the side effects of immunotherapy to be aware of, and how do you manage them?

Dr. Postow: Immunotherapy enhances the body’s immune system, and our hope is that this results in improved antitumor immunity against the malignancy. Unfortunately, this activation of the immune system can also result in reactivity against tissues not involved in the malignancy, creating important side effects. And since patients often require immunosuppression for the treatment of immune-related side effects, the potential for the development of opportunistic infections is important to keep in mind.

Inflammatory pneumonitis is particularly relevant for antibodies that block the PD-1 axis. A few patients, unfortunately, died from complications of pneumonitis in one of the phase I trials. However, with increasing recognition and prompt treatment using immunosuppressants, we believe that this potential side effect can be effectively managed. The number of patients who experience pneumonitis is very low, particularly those in whom it occurs to any significant degree.

Renal insufficiency is another side effect—elevated creatinine levels have been associated with the PD-1 agents. Colitis and diarrhea seem to be more of a problem with CTLA-4 blockade than with PD-1 blocking agents.

The main point to remember, though, is that all of these agents can cause immune-related adverse events, which are generally easily managed with prompt recognition and the initiation of steroids or other immunosuppressants. Long-term sequelae are generally extremely mild, if they occur at all.

No maximum tolerated dose has been established in dose-escalation studies with PD-1 agents. These drugs are very well tolerated because the mechanism for adverse effects is different from that which occurs in chemotherapy or targeted therapy.   

Measuring response to immunotherapy

Dr. Nimeh: How is response to immunotherapy measured, and how is “success” defined?

Dr. Postow: Ultimately, we will assess the response to immunotherapy differently from the methods we have been using up to this point. Right now, however, response to immunotherapy is assessed using traditional radiographic response criteria, such as those applied to other investigational agents. Basically, these are the modified World Health Organization response criteria or the RECIST criteria.

Traditional response endpoints, apparent on CT scans or PET scans, can often be misleading and potentially underestimate the long-term survival benefits accrued with immunotherapies. The reason is that the patterns of response that occur with immunotherapy are different from those observed with traditional chemotherapy. For example, with immunotherapy, new lesions may appear in the presence of an otherwise decreasing tumor burden, and there may even be an apparent worsening of overall tumor burden, prior to ultimate shrinkage of the tumor burden and a response.

The immune-related response criteria have been investigated for patients treated with ipilimumab (an anti−CTLA-4 blocking antibody now approved by the FDA), and it was proposed that a novel set of response criteria should be applied to that drug. In fact, the novel immune-related response criteria appeared to better approximate the long-term survival benefits of the drug as compared with traditional radiographic response endpoints. The newly proposed response criteria still need to undergo prospective evaluation. Nevertheless, immunotherapies, particularly the PD-1 agents, demonstrate high response rates even with traditional radiographic response criteria, such as RECIST.

We are still struggling to establish the best surrogates to apply in early-phase trials and to ascertain how well these surrogates correlate with overall survival. Overall survival, therefore, remains the most important endpoint in clinical trials evaluating the immunologic agents. Interestingly, a greater number of patients have achieved long-term survival after treatment with ipilimumab than were considered to have responded by traditional radiographic response criteria.

Treatment regimens in immunotherapy

Dr. Nimeh: With new treatment approaches emerging, what is the potential for combining immunotherapies—for example, ipilimumab and granulocyte-macrophage colony-stimulating factor (GM-CSF)—or adding targeted therapy?

Dr. Postow: Many new agents appear to be promising as monotherapies. It is very exciting to think about the possibility of additive (or potentially synergistic) benefits if we combine more than one in appropriate and rational ways.

At ASCO this year, Dr. Stephen Hodi presented data which showed that patients who received ipilimumab 10 mg/kg in combination with GM-CSF had improved overall survival as compared with patients who received ipilimumab 10 mg/kg alone.3 The results were consistent with those from preclinical evaluations in mice. This combination treatment demonstrates the potential promise of combining these immunologic agents.

We reported in The New England Journal of Medicine,4 and also presented at ASCO this year,5 that, in a phase I trial involving a small number of patients, the combination of nivolumab with ipilimumab resulted in a very impressive response rate.

Whether or not these responses to combination nivolumab and ipilimumab (which have been durable) translate into long-term overall survival benefit is the subject of an ongoing phase III study. At this juncture, we do not yet know whether it is better to combine nivolumab and ipilimumab initially or to sequence them, one followed by the other. Patients can respond to nivolumab even if they have not responded to ipilimumab and vice-versa. We are hopeful that the large-scale phase III trials will answer these questions regarding the relative merits of combination therapy vs monotherapy. Combinations of targeted therapy and immunotherapy are also very exciting to investigate. Several prior evaluations6,7 have suggested that treatments such as BRAF inhibitors can result in immunologic effects that may be additive or synergistic when combined with immunotherapy.

We conducted a phase I trial in which we combined vemurafenib with ipilimumab.8 Unfortunately, the trial was discontinued because the rate of hepatotoxicity was too high. One of the many lessons we learned from that trial was the importance of carefully evaluating combinations of targeted therapy with immunotherapy in early-phase clinical trials, in which dosing and scheduling are very carefully monitored. It is possible that sequencing these agents, or using specific combinations, will be more tolerable and possibly beneficial.

One ongoing study is evaluating the use of dabrafenib and ipilimumab, with or without the MEK inhibitor trametinib.9 We are hopeful that this study will provide some additional information on the possibility of combining targeted agents with immunotherapy for patients with advanced melanoma. At this point, we would not recommend combining immunotherapy and targeted therapy outside of the context of a clinical trial. We encourage the enrollment of patients in such trials.

  • References
    1. Topalian SL, Hodi FS, Brahmer JR, et al. Safety, activity, and immune correlates of anti-PD-1 antibody in cancer. N Engl J Med. 2012;366(26):2443-2454.

    2. Sznol M, Kluger HM, Hodi FS, et al. Survival and long-term follow-up of safety and response in patients (pts) with advanced melanoma (MEL) in a phase I trial of nivolumab (anti-PD-1; BMS-936558; ONO-4538). Paper presented at: American Society of Clinical Oncology; May 31-June 4, 2013; Chicago, Illinois. J Clin Oncol. 2013(suppl; abstr CRA9006).

    3. Hodi SF, Lee SJ, McDermott DF, et al. Multicenter, randomized phase II trial of Gm-CSf (GM) and ipilimumab (Ipi) versus Ipi alone in metastatic melanoma: E1608. J Clin Oncol. 2013(suppl; abstr CRA9007).

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

    5. Wolchok JD, Kluger HM, Callahan MK, et al. Safety and clinical activity of nivolumab (anti-PD-1, BMS-936558, ONO-4538) in combination with ipilimumab in patients (pts) with advanced melanoma (MEL). Paper presented at: American Society of Clinical Oncology; May 31-June 4, 2013; Chicago, Illinois. J Clin Oncol. 2013(suppl; abstr 9012).

    6. Frederick DT, Piris A, Cogdill AP, et al. BRAF inhibition is associated with enhanced melanoma antigen expression and a more favorable tumor microenvironment in patients with metastatic melanoma. Clin Cancer Res. 2013;19(5):1225-1231.

    7. Comin-Anduix B, Chodon T, Sazegar H, et al. The oncogenic BRAF kinase inhibitor PLX4032/RG7204 does not affect the viability or function of human lymphocytes across a wide range of concentrations. Clin Cancer Res. 2010;16(24):6040-6048.

    8. Ribas A, Hodi SF, Callahan C, et al. Hepatotoxicity with Combination of Vemurafenib and Ipilimumab [correspondence].N Engl J Med 2013;368(14):1365-1366.

    9. Phase I study of the BRAF inhibitor dabrafenib +/− MEK inhibitor trametinib in combination with ipilimumab for V600E/K mutation positive metastatic or unresectable melanoma. NCT01767454. http://clinicaltrials.gov/ct2/show/NCT01767454?term=dabrafenib+and+ipili.... Accessed July 14, 2013.

 

 

Copyright © 2013 Elsevier. All rights reserved.

 

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DeniseK's picture
Replies 21
Last reply 8/7/2013 - 9:28am

Hi Everyone,

I was just diagnosed with mm on June 2, 2011.  Surgery and sentinal lymph node removal on June 8, 2011.

Pathology report came back as follows. 

Nodular Malignant Melanoma

Surface measurement 2.7 x 2.7

Breslow Depth 14mm

Clarks level V

Sparse Lymphocytic infiltrate at periphery of Melanoma

Ulceration present

Mitoses 4/mm

Skin margins and deep margins negative for melanoma

Melanoma 1.5 cm to deep margin__________________________

My doctor said I was Stage IIC with high risk reoccurrence and wanted me to research diferent options for treatment.

I understand the clarks level V isn't good and the breslow depth was high but what does the ulceration mean and why is it bad?

If anyone understands what Mitoses 4/mm means let me know too!!  Thanks for your help!!

 

Denise 

Cancer Cannot cripple love, silence courage, destroy friendship, shatter hope or conquer the spirit.

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DonnaK's picture
Replies 13
Last reply 8/7/2013 - 9:22am

My husband began interferon treatment on Monday.  The first infusion hit him almost immediately after treatment and he had serious chills and a fever, but managed to sleep it all off and get to work the next morning.  Today was round two, and while he didn't get the same chills as yesterday, he has pretty much been incapacitated since we got home from the hospital.  So, I guess I'm wondering if this is par for the course, or if his symptoms will subside a bit.  I think we can take this for a month but, if this continues beyond that, it will be as if we lost a year of his life where he could have been otherwise healthy. For past interferon patients, what is life like beyond the first month?  Are you generally able to live your lives, or do you feel like your life is on hold until treatment is complete?  

I am so grateful for any responses. I know this is a personal decision, and I'm not looking for people to bash interferon. I guess I'm just looking to see if there is hope around the corner.  At this point, I'm having a hard time believing this is the right decision for us...

Thank you.

Donna

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Replies by: Anonymous, JerryfromFauq, POW, Janner

http://www.medicalnewstoday.com/releases/264401.php?nfid=108115
Gene test identifies non-metastatic melanoma patients at high risk of recurrence.    Article Date: 06 Aug 2013 - 2:00 PDT

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

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H555's picture
Replies 7
Last reply 8/7/2013 - 7:28am

i'm just about to begin week 3 of high dose Inteferon IV and am totally whipped. it's all I can do to get up after sleeping 12 hours. i've started taking a nap within 2 hours of getting up. I've got no appetitie but am drinking protein shakes and peanut butter and toast. The meds are managing the side effects ok. i had a very high fever and severe chills after the first treatment but only slight chillls the following monday. my biggest challenge is appetite and fatigue. does anyone have any tips for getting thru the next two weeks? thankyou.

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eaca's picture
Replies 41
Last reply 8/7/2013 - 4:39am

I just had a consultation with my medical oncologist today during which we discussed the Interferon decision.  The options for me are:  Wait and Watch; classic Interferon treatment; Pegylated Interferon; try to get on a trial at MD Anderson combining Peg-Interferon and peptide vaccine (gp100).  I've read up here on what others have had to say on Interferon or not, but there doesn't seem to be too much experience with the pegylated version or the vaccine.  I'm 'only' stage II, but relatively high risk because of the mitotic rate of my primary.  In the end I know this will come down to a very personal choice, but I thought I'd put it out there for any thoughts others might have.

After my relief over being clear after surgery, I'm now feeling confused and worried again.  Big choices to be made.  Thanks in advance for any input!

Elisa

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