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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Well, I guess the good news is that not ALL melanoma cancer cells are cancer stem cells, as one recent study posited, or express the protein CD 271 ...... Now, if they can find or develop something which can target melanoma cells expressing this protein, how great would would that be ?  ..... I guess we should take heart in that the first step in defeating any foe is usually Sun Tzu's maxim "Know Your Enemy"....even though this particular enemy can look like Arnold in The Terminator at times.....Hawaii Bob, Stage IIA

 

Melanoma-Initiating Cell IdentifiedScienceDaily (July 1, 2010) — Scientists at the Stanford University School of Medicine have identified a cancer-initiating cell in human melanomas. The finding is significant because the existence of such a cell in the aggressive skin cancer has been a source of debate. It may also explain why current immunotherapies are largely unsuccessful in preventing disease recurrence in human patients. "These cells lack the traditional melanoma cell surface markers targeted by these treatments," said post-doctoral fellow Alexander Boiko, PhD. "Without wiping out the cells at the root of the cancer, the treatment will fail."

Boiko is the first author of the research, which will be published in the July 1 issue of Nature. He works in the laboratory of Irving Weissman, MD, the director of Stanford's Institute for Stem Cell Biology and Regenerative Medicine. Weissman is the medical school's Virginia & D.K. Ludwig Professor for Clinical Investigation in Cancer Research and the senior author of the research. He is also a member of the Stanford Cancer Center.The cancer stem cell theory holds that, like queen bees in a hive, only a subset of cancer cells are at the root of the tumor's growth. These cells can both self-renew (that is, make more of themselves) and differentiate into other tumor cell types.

Any therapy that doesn't wipe out these elite cancer stem, or initiating, cells has no chance of completely eradicating the disease even if it destroys nearly all other tumor cells. That's why, say proponents, it can be relatively easy to get a patient into remission, but extremely difficult to prevent the cancer stem cells from roaring back and causing a relapse months or years later. Cancer stem cells were first identified in blood cancers, but have since been identified in a number of solid tumors including bladder, brain, breast and colon cancers. Previous studies in the laboratory of assistant professor of radiation oncology Maximilian Diehn, MD, PhD, in collaboration with the laboratories of Weissman and Stanford colleague Michael Clarke, MD, have indicated that cancer stem cells may be more resistant than other cancer cells to many common treatments like radiation and some chemotherapies. Clarke is the Karel H. and Avice N. Beekhuis Professor in Cancer Biology at the medical school and both Diehn and Clarke are members of the Stanford Cancer Center.

Although a growing body of evidence seems to support the cancer stem cell hypothesis, melanoma has remained a conundrum. A University of Michigan study in 2008 found that as many as one in four melanoma cells could cause cancers in immune compromised mice, suggesting that there may not be a particularly privileged subset of cancer stem cells in this tumor type. Boiko set out to solve the mystery.  "I didn't know if melanoma would in fact have the cancer-initiating cells," said Boiko. "I was completely unbiased, so I was actually sort of surprised to find such a clear-cut answer. It fits exactly what's been discovered in the studies of other solid tumors."

To conduct the study, Boiko analyzed cell surface markers on primary melanoma tumor samples taken directly from patients at the Stanford Cancer Center. In this way, he avoided having to grow the cells for a long period of time in the lab. Continuous culturing, or passage, of cancer cells often gives the cells time to evolve and change in ways that might not accurately reflect their composition in melanoma patients. He found that one protein, called CD271, was always expressed on only a fraction of the cells in the human melanoma samples tested: The proportion of cells expressing CD271 varied in the samples from 2.5 to 41 percent of the total cell population; the marker appeared on a mean of 16.7 percent of cells in the samples.

This was interesting because CD271 was previously identified as a marker that identifies a group of cells called the neural crest stem cells. These cells are unique in that they are a multipotent, migratory cell population that becomes many cell types during development including melanocytes (cells responsible for skin pigmentation), bone, smooth muscle, neurons, and cartilage in the head and face. When Boiko transplanted the melanoma cells from nine human samples into laboratory mice with severely compromised immune systems, he found that the cells expressing CD271 on their surface were much more likely to cause cancers in the recipients than those from the same tumor that didn't express the marker (70 percent versus 7 percent, respectively). And all but one of the newly induced tumors arising from the transplantation of the CD271-positive cells went on to develop a population of a mixture of CD271-expressing and non-expressing cells -- indicating that the cells with the marker were both self-renewing and differentiating into other types of tumor cells.

Article continues at the link

 

 http://www.sciencedaily.com/releases/2010/06/100630132754.htm

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Shelby - MRF's picture
Replies 11
Last reply 8/19/2010 - 3:50pm

Hello everyone!  I wanted to introduce myself to you before the premier of The Big C tonight on Showtime at 10:30 ET/PT.  I am the new Health Educator at the MRF and I will be online throughout the show to chat with you and/or hear your feedback.  I am just beginning my second week with the foundation and I am learning a lot and really looking forward to knowing each of you.  My main role at MRF will be to improve the means by which we are educating patients, both through face-to-face and electronic forms of communication.  We are really trying to connect with every single patient we can and provide them with the best information possible.  Have a wonderful day and I hope to hear your feedback tonight! 

Shelby Moneer

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Combined BRAF-Targeted and Immunotherapy Shows Promise for Melanoma Treatment

ScienceDaily (June 15, 2010) — Combined targeted therapy against the BRAF/MAPK pathway with immunotherapy shows promise as a new therapeutic approach for the treatment of melanoma, according to results of a preclinical study published in Cancer Research, a journal of the American Association for Cancer Research. 

"Our results provide preclinical evidence for the rational combination of BRAF-targeted therapy and immunotherapy in the treatment of this most dangerous type of skin cancer," said lead researcher Jennifer A. Wargo, M.D., division of surgical oncology at Massachusetts General Hospital, Boston.

"By blocking the oncogenic BRAF, tumor antigen expression may be restored. This would make the melanoma tumors susceptible to strategies incorporating immunotherapy," she said.

Previous studies have shown that melanoma treatment with selective BRAF inhibitors are very effective and result in a high initial response rate, but the response is temporary. An alternative approach would be to combine other agents and extend the duration of treatment response.

Using biopsies of melanoma tumors, the researchers investigated the effects of mitogen-activated protein kinase (MAPK) pathway inhibition vs. selective inhibition of BRAF-V600E on T-cell function.

Inhibition of the MAPK pathway with a specific inhibitor of BRAF-V600E resulted in increased expression of antigens, which was associated with improved recognition by antigen-specific T-cell. T-cell function was not compromised after treatment with BRAF-V600E.

Mario Colombo, Ph.D., director of molecular immunology at the Italian National Cancer Institute and senior editor for Cancer Research, said these results advance cancer research by offering new arguments to sustain the combination of selective targeted therapy with immunotherapy.

"This study shows the need for considering the effect of off-targeted drug therapy on the many aspects of host immune response to make real the combination of chemo- and immunotherapy," Colombo said. "It also prompts the idea of performing vaccination in the attempt to eradicate the disease and prevent recurrence."

Several clinical trials are underway using agents that selectively inhibit BRAF-V600E in patients with metastatic melanoma. These studies have shown impressive response rates, though durability of response remains an issue, according to Wargo.

Results of this study provide a basis for combining this type of therapy with immunotherapy, with the goal of improving durability of responses.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Association for Cancer Research.

 

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New Treatment Method Safe, Effective for Advanced Melanoma Patients, Study Suggests

ScienceDaily (June 7, 2010) — Patients undergoing treatment for melanoma that has spread to the liver may respond well to chemotherapy delivered directly into the liver's blood vessels, according to a study sponsored by the National Cancer Institute and Delcath Systems Inc., and led by James F. Pingpank, M.D., associate professor of surgery, University of Pittsburgh School of Medicine, and surgical oncologist with UPMC Cancer Centers. 

The results were presented in an oral presentation on June 5 in Chicago at the 46th annual meeting of the American Society of Clinical Oncology (ASCO).

"Once melanoma spreads to the liver, a patient's life expectancy typically ranges from six to nine months," said Dr. Pingpank. "We hoped this study would not only show an increase in progression-free survival rates for these patients, but also lead to a standard of care for the disease."

The phase III trial enrolled 93 patients from 10 different sites across the country between February 2006 and October 2009. Its primary goal was to double the length of hepatic progression-free survival for patients with melanoma that had spread to the liver. Patients received either percutaneous hepatic perfusion (PHP) with the drug melphalan, meaning the chemotherapy was delivered directly into the blood vessels of the liver, or the treatment considered the best alternative regimen by their treating physician. If a patient not receiving PHP had disease progression, he or she could cross over to the PHP arm of the trial.

"Not only did we achieve our goal, we surpassed it," said Dr. Pingpank. "This is particularly exciting because so far oncologists haven't been able to recommend a standard of care for patients with melanoma that has spread to the liver. PHP appears to control tumors in the liver and extend life expectancy for these patients, whether their melanoma began as skin cancer or as ocular melanoma, a less common form of the disease that starts in the eye. Fifty percent of ocular melanoma patients will experience liver metastasis, so these findings are crucial for them."

Melanoma is a rare form of cancer, but it causes the majority of skin cancer-related deaths. Each year, approximately 160,000 new cases are diagnosed worldwide. Ocular melanoma will be diagnosed in approximately 2,500 adults this year.

Other sites involved in the study include the Surgery Branch of the NCI, Bethesda, Md.; John Wayne Cancer Institute, Santa Monica, Calif.; H.Lee Moffitt Cancer Center, Tampa, Fla.; University School of Maryland Medicine, Baltimore; The University of Texas M.D. Anderson Cancer Center, Houston; Atlantic Melanoma Center, Morristown, N.J.; Rad Imaging Associates, Englewood, Colo.; Albany Medical Center Hospital, Albany, N.Y.; and St. Luke's Hospital and Health Network in Bethlehem, Pa.

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From Washington University in St. Louis, MO -- where I was treated for my primary almost two years ago (Siteman Cancer Center, Wash U).... This technology is amazing.   Regards, Hawaii Bob

 

Advance Toward Earlier Detection of Melanoma

 

This skin tumor (top) is shown after treatment with a new contrast agent that can improve the visualization of skin cancer cells (bottom) using an advanced medical imaging device. (Credit: American Chemical Society)

ScienceDaily (Aug. 11, 2010) — Melanoma is one of the less common types of skin cncer but it accounts for the majority of the skin cancer deaths (about 75 percent). 

The five-year survival rate for early stage melanoma is very high (98 percent), but the rate drops precipitously if the cancer is detected late or there is recurrence.

So a great deal rides on the accuracy of the initial surgery, where the goal is to remove as little tissue as possible while obtaining "clean margins" all around the tumor.

So far no imaging technique has been up to the task of defining the melanoma's boundaries accurately enough to guide surgery. Instead surgeons tend to cut well beyond the visible margins of the lesion in order to be certain they remove all the malignant tissue.

Two scientists at Washington University in St. Louis have developed technologies that together promise to solve this difficult problem.

Their solution, described in the July issue of ACS Nano, combines an imaging technique developed by Lihong Wang, PhD, the Gene K. Beare Distinguished Professor of Biomedical Engineering, and a contrast agent developed by Younan Xia, PhD, the James M. McKelvey Professor of Biomedical Engineering.

Together the imaging technique and contrast agent produce images of startling three-dimensional clarity.

Photoacoustic tomography

The imaging technique is based on the photoacoustic effect discovered by Alexander Graham Bell 100 years ago. Bell exploited the effect in what he considered his greatest invention ever, the photophone, which converted sound to light, transmitted the light and then converted it back to sound at the receiver.

(The public preferred the telephone to the photophone, by some facetious accounts because they just didn't believe wireless transmission was really possible.)

In Bell's effect, the absorption of light heats a material slightly, typically by a matter of millikelvins, and the temperature rise causes thermoelastic expansion.

"Much the same thing happens," says Wang "when you heat a balloon and it expands."

If the light is pulsed at the right frequency, the material will expand and contract, generating a sound wave.

"We detect the sound signal outside the tissue, and from there on, it's a mathematical problem," says Wang. "We use a computer to reconstruct an image."

"We're essentially listening to a structure instead of looking at it," says Wang.

"Using pure optical imaging, it is hard to look deep into tissues because light is absorbed and scattered," Wang explains. "The useful photons run out of juice within one millimeter."

Photoacoustic tomography (PAT) can detect deep structures that strongly absorb light because sound scatters much less than light in tissue.

"PAT improves tissue transparency by two to three orders of magnitude," says Wang.

Moreover, it's a lot safer than other means of deep imaging. It uses photons whose energy is only a couple of electron-volts, whereas X-rays have energies in the thousands of electron-volts. Positron emission tomography (PET) also requires high-energy photons, Wang says.

A smart contrast agent

Photoacoustic images of biological tissue can be made without the use of contrast agents, particularly if tissues are pigmented by molecules like hemoglobin or melanin.

Still, photoacoustic images of melanomas are fuzzy and vague around the edges. To improve the contrast between the malignant and normal tissue, Xia loads the malignant tissue with gold.

"Gold is much better at scattering and absorbing light than biological materials," Xia says. "One gold nanocage absorbs as much light as a million melanin molecules," says Xia.

Xia's contrast agent consists of hollow gold cages, so tiny they can only be seen through the color they collectively lend to the liquid in which they float.

By altering the size and geometry of the particles, they can be tuned to absorb or scatter light over a wide range of wavelengths.

In this way the nanoparticles behave quite differently than bulk gold.

For photoacoustic imaging, Xia's team tunes the nanocages to absorb strongly at 780 nanometers, a wavelength that falls within a narrow window of tissue transparency in the near-infrared.

Light in this sweet spot can penetrate as deep as several inches in the body.

Once injected, the gold particles naturally tend to accumulate in tumors because the cells that line a tumor's blood vessels are disorganized and leaky.

But Xia has dramatically increased the uptake rate by decorating the nanoparticles with a hormone that binds to hormone receptors on the melanoma's cells.

The molecule is alpha-melanocyte-stimulating hormone, slightly altered to make it more stable in the body. This hormone normally stimulates the production and release of the brown pigment melanin in the skin and hair.

As is true in many types of cancers, this hormone seems to stimulate the growth of cancerous cells, which produce more hormone receptors than normal cells.

In experiments with mice, melanomas took up four times as many "functionalized" nanocages than nanocages coated with an inert chemical. With the contrast agent, the photoacoustic signal from the melanoma was 36 percent stronger.

But seeing is believing. Subcutaneous mouse melanomas barely visible to the unaided eye show up clearly in the photoacoustic images, their subterranean peninsulas and islands of malignancy starkly revealed.

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amybusby's picture
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Last reply 8/18/2010 - 10:34pm
Replies by: Kevin from Atlanta

Now that my spinal fluid has been cleared up, my leptominingial mets are getting a bit worse (lining of my brain).  So Dr. Papa thinks I should do a 10 day course of WBR along with Temodar.  I was expecting that would probably be the results / recommendations.  Problem is how much of the T. cost is my insurance going to cover?  Hopefully I'll know tomorrow, but since I needed to start it tonight, we're already behind schedule.  Has anyone had any success with assistance?

I've heard it's not too bad but I'd like any advice / input on the WBR / T. treatment too!

Thanks,

Amy

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Joyce's picture
Replies 6
Last reply 8/18/2010 - 9:34pm

Dick and I went to his oncologist at Ma General today. As we posted he is 4 years NED from stage 4. For the very first time in the years we have been fighting this beast (2002-stage 4) the doctor was hopeful and excited. He said they are on the verge of so many break thrus. He said the anti-ctla 4 drug Dick had had 4 years ago was unknown back then but has become cutting edge. And Dick was in one of the original trials.  Our original oncologist whom we had seen in Feb 2003 had given us very little hope that Dick would be around in 5 years. There was nothing that really stopped the spread of  melanoma. Well, today the attitude was entirely different. While, there are some people who sadly don't respond to anything, there are a lot more who do respond now. Some are given a little more quality time and others go into remission.

 

Joyce from MA (formerly Dick's wife Dick stage 4)

'

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KatyWI's picture
Replies 1
Last reply 8/18/2010 - 9:08pm
Replies by: debbieVA

Is anyone else attending this Proleukin patient summit in San Diego in Septmeber?  My doctor's nurse told me about it.  I agreed to attend and wonder whether I'll meet any of you there.

KatyWI

Just keep going!

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lovingwifedeb's picture
Replies 3
Last reply 8/18/2010 - 4:37pm

Has anyone ever heard of this?

Husband's melanoma tumor (2 inches long) was in an enlarged lymph node in the groin area as a secondary sight, primary melanoma source was never found as such, not by any mole or freckle on body.

Surgery is completed. All other lymph nodes in surrounding area also taken and were all tested as non-cancerous.

Since Primary tumor has not been found, is it recessed? Occult? Just what has happened?

Suggestions for treatment?

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Nancy's picture
Replies 7
Last reply 8/18/2010 - 3:38pm

Buddy was hospitalized yesterday - his blood count was 8 - so they're keeping him overnight and transfusing.  Hopefully, when they check him this morning, he'll have the 'Blood of an Irishman" flowing through his veins, and will get to come home.  He had the IPI treatment last Tuesday and I think it may have made him a lilttle weak...but we'll get him patched up soon and back in the orchard (I Hope).

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Nancy's picture
Replies 7
Last reply 8/18/2010 - 3:27pm

I've heard you don't know if one is respondng to IPI for three months.  Buddy had one tumor shrink and the others that were measured increase in size.  He's had no side effects, the fatigue was there already due to craniology and WBR--He has numerous tumors - liver, lungs, spleen and the brain mets.  Dr. said he is anemic, will have blood transfusion next week.  Also, if he has any more imbalance while walking, he will need MRI - said he could get gamma knife and still continue with IPI- do you think they would do a gamma knife to brain mets if he has more than 3?  Is there a pill or something for blood - H&H is 11 - going south quickly, will transfuse at 9 - has blood work Sunday.  Is there anything to do to prevent a seizure that we are not doing now? 

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tricialeigh44's picture
Replies 1
Last reply 8/18/2010 - 10:46am
Replies by: lovingwifedeb

I just wanted to thank you all. My aunt found this forum and linked it to me. I have been trying to read as many posts as possible (with a 2.5 year old and 13 week old). My mom was diagnosed with stage 4 malignant melanoma  a few weeks ago (July 28 at 3pm to be exact)...who could ever forget an appointment like that.

I have learned so much from all of your posts and have been able to further investigate different therapies available to my mom. Most importantly I have realized that we are not alone in this horrible nightmare. There are good people all over the world fighting this disease.

 

I just wanted to thank you for giving me strength for my mom and my family. Keep fighting, there are so many treatments coming out for this disease and I am sure a cure is on its way!

Tricia

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susanlee's picture
Replies 2
Last reply 8/18/2010 - 10:10am
Replies by: Phil S, babybluiz

I wanted to post a message to thank everyone for the words of support and encouragement you have given regularly. I have been viewing the posts on this board since my diagnosis mid-May 2010. I have acral letiginous melanoma of my left thumb. SNB and amputation of thumb were completed in June 2010. SNB was negative thankfully.  Chest x-ray, abdominal ultrasound and blood work were all within normal limits. Tumor size (7.9 mm) and mitotic rate (8/mm2) however were concerns for my doctors.

I am having a CT scan tomorrow to establish a baseline and will be starting Interferon this coming Monday. I am not sure how I will react and how quickly the side effects will impact me. I know it varies from person to person but would appreciate any information you could provide.

Thanks

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joy_'s picture
Replies 4
Last reply 8/18/2010 - 9:53am

My husband was hoping to qualify for the Derma study, but we found out today that he didn't.  He's currently stage IIIc and we are looking into other treatment options.  This looks to be a Phase 1 study, and I am curious if anyone out there knows anything about it or has received this treatment.  I've searched the board and couldn't find anything about it.  Maybe it is known by another name?

Tracy

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Joyce's picture
Replies 2
Last reply 8/18/2010 - 9:03am
Replies by: ValinMtl, triciad

Dick just had his scans and now has been NED for 4 years. He had his last surgery in June, 2006. He took the vaccine made out of his tumor and GMC-SF and then had 4 infusions on anti ctla-4. I have been known as Dick's wife (Dick stage 4) but I think that changed with the new format.

Joyce from MA

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