Bristol-Meyer Squibb has a lot to Explain!!Melanoma..Jim Breitfeller

Bristol-Meyer Squibb has a lot to Explain!!!!!!

Guess what, Bristol-Meyer Squibb is not as ethical as they would like you to think. Bristol-Meyer Squibb and Medarex which is now a subsidiary of Bristol after the takeover, stopped the compassionate Use for Ipilimumab Anti-CTLA-4 Blockage. This happen in September of 2008 it has been a year without this compassionate use. I know that is does not take a year to manufacture Monoclonal antibodies. It takes about three months to produce a batch of them. So why is there still no compassionate use?

Well, I got to thinking that they (Bristol Meyer Squibb) must be producing it and if so it would show up as Clinical Trials. So I crossed referenced Clinical trials starting after September 2008. Low and behold, I found NEW CLINICAL TRIALS. This means Bristol-Meyer Squibb have been scamming the Melanoma patients that need it the most. The ones that have run out of options and Ipilimumab was their last hope for survival.


Here are the trials:

Study of Ipilimumab and Dasatinib Combination Therapy in Patients With Chronic or Accelerated Chronic Myeloid Leukemia

Start Date: August 2009
Estimated Study Completion Date: Feb 2011
Estimated Enrollment: 30
ClinicalTrials.gov Identifier: NCT00732186


Ipilimumab +/- Vaccine Therapy in Treating Patients With Locally Advanced, Unresectable or Metastatic Pancreatic Cancer

Start Date: February 2009
Estimated Study Completion Date: Feb 2013
Estimated Enrollment: 30
ClinicalTrials.gov Identifier: NCT00836407

Bevacizumab Plus Ipilimumab in Patients With Unresectable Stage III or IV Melanoma

Start Date: February 2009
Estimated Study Completion Date: Feb 2011
Estimated Enrollment: 33
ClinicalTrials.gov Identifier: NCT00790010

Laboratory-Treated T Cells With or Without Ipilimumab in Treating Patients With Metastatic Melanoma

Start Date: February 2009
Estimated Study Completion Date: Feb 2011
Estimated Enrollment: 30
ClinicalTrials.gov Identifier: NCT00871481

Study of Immunotherapy to Treat Advanced Prostate Cancer

Start Date: May 2009
Estimated Study Completion Date: December 2012
Estimated Enrollment: 800
ClinicalTrials.gov Identifier: NCT00861614


Further study details as provided by Bristol-Myers Squibb:

These are all trials that were started after the halting of the compassionate Use. Bristol-Meyer Squibb thinks we the Melanoma Patients are expendable so they continued there quest to seek out new uses for the Drug.

Get a bigger bang for the buck.

They already know it will work well with Melanoma so why not find other uses.

Base on my calculation, 923 late stage Melanoma Patients were denied the drug while Bristol–Meyer Squibb continued to apply and start up new trials.

Bristol-Meyer Squibb Quote:

“What sets us apart? We believe it's our commitment to patients with serious diseases, our focus on finding innovative medicines that combat those diseases, and our dedication to extending and enhancing human life.”

All Lip Service!!!!!!

Where are the Ethical Standards??

BMS did not make the 2009 World’s Most Ethical Companies

“The World’s Most Ethical Companies are the ones that go above and beyond legal minimums, bring about innovative new ideas to expand the public well being, work on reducing their carbon footprint rather than contributing to green washing and won’t be found next to the words “Billion Dollar Fine” in newspaper headlines any time in the near future. These are the companies that stand out among the competition in their industry.”

Source: Ethishere.com

Jimmy B



Take Care,

Jimmy B

Watch Dr Jeff Weber, Moffitt Cancer Center, Tampa, Florida, USA, ANTI-CTLA-4: A new immunological approach on ecancer tv. Cancer journal: online cancer news, clinical oncology research, cancer information and latest cancer studies - open access cancer journal: ecancermedicalscience | ecancermedicalscience

Watch Dr Jeff Weber, Moffitt Cancer Center, Tampa, Florida, USA, ANTI-CTLA-4: A new immunological approach on ecancer tv. Cancer journal: online cancer news, clinical oncology research, cancer information and latest cancer studies - open access cancer journal: ecancermedicalscience ecancermedicalscience

Shared via AddThis

MELANOMA: NEW THERAPY WITH IPILIMUMAB, VIDEO INTERVIEW PROF.A.EGGERMONT at ECCO September 2009

We are seeing the fruits of our Labor

Video interview with prof.Alexander Eggermont, Ecco Oncology President at 15 Ecco Esmo 34 European Oncology Congress in Berlin, september 2009.

You need to shut off my playlist to stop the music before you listen to the video.




Take Care,

Jimmy B

Bristol's String of Pearls are Shining!!

FDA NEWS RELEASE
For Immediate Release: Sept. 25, 2009

Media Inquiries: Karen Riley, 301-796-4674, karen.riley@fda.hhs.gov
Consumer Inquiries: 888-INFO-FDA

FDA Approves New Drug to Treat Psoriasis

The U.S. Food and Drug Administration today approved Stelara (ustekinumab), a biologic product for adults who have a moderate to severe form of psoriasis.

Plaque psoriasis is an immune system disorder that results in the rapid overproduction of skin cells. About 6 million people in the United States have plaque psoriasis which is characterized by thickened patches of inflamed, red skin, often covered with silvery scales.

“This approval provides an alternative treatment for people with plaque psoriasis, which can cause significant physical discomfort from pain and itching and result in poor self-image for people who are self-conscious about their appearance,” said Julie Beitz, M.D., director, Office of Drug Evaluation III, in the FDA’s Center for Drug Evaluation and Research.

Stelara is a monoclonal antibody, a laboratory-produced molecule that mimics the body’s own antibodies that are produced as part of the immune system. The biologic treats psoriasis by blocking the action of two proteins which contribute to the overproduction of skin cells and inflammation.

Three studies of 2,266 patients evaluated the biologic’s safety and effectiveness.

Since Stelara reduces the immune system’s ability to fight infections, the product poses a risk of infection. Serious infections have been reported in patients receiving the product and some of them have lead to hospitalization. These infections were caused by viruses, fungi, or bacteria that have spread throughout the body. There may also be an increased risk of developing cancer.

The FDA is requiring a risk evaluation and mitigation strategy or REMS for Stelara that includes a communication plan targeted to healthcare providers and a medication guide for patients.

Stelara is manufactured by Centocor Ortho Biotech Inc. of Horsham, Pa., a wholly-owned subsidiary of Johnson & Johnson of New Brunswick, N.J.

Well Medarex is the partner who developed the antibody, (ustekinumab).

We shall soon hear about Ipilimumab, I hope

Bristol-Meyer Squibb just bought out Medarex in what I would call a give away by the Board of Directors and the Top Management of Medarex.

My guess, Bristol had information on Stelara proir to buying out Medarex.

The Pearl Neckace Lives On!!!!!!!!

I believe each pearl represents an antibody or Drug that is commercialized and FDA approved.

commercialized.. Definition --To apply methods of business to for profit.

BMY will get some royalites that can fund their war chest.

Check Mate!!!!!!!

Take Care,

Jimmy B

Bristol-Myers Squibb at Morgan Stanley Global Healthcare Conference 9/14/2009..Melanoma .Jim Breitfeller

Bristol-Myers Squibb at Morgan Stanley Global Healthcare Conference 9/14/2009

If you go to Bristol-Myers Squibb's website and click on investor, you will see:

Events and PresentationsBristol-Myers Squibb at Morgan Stanley Global Healthcare Conference
Monday, September 14, 2009
Webcast replay

If you sign up and play the webcast, you get the feeling that it all comes down to greed and money in my opinion. Market share, Patients, Doctors all in one breath.

Have patient become a comodity? We will vote with our feet and voices.

When they say, “What sets us apart? We believe it's our commitment to patients with serious diseases, our focus on finding innovative medicines that combat those diseases, and our dedication to extending and enhancing human life.”

All smoke and mirrors!!!!!!!

But if you listen and reach 25.55 minutes into the webcast, there is a question on Medarex and Ipilimumab. Fully human anti CTLA-4 monoclonal antibody in advanced clinical trials, Metastatic Melanoma. Phase III Data Overall Suvival data will be out shortly. With these results (I believe will be positive) in hand, I believe that Bristol-Myers Squibb (BMY) will apply for a biological licence from the FDA.

Biological products often represent the cutting edge of medical science and research. Also known as biologics, these products replicate natural substances such as enzymes, antibodies, or hormones in our bodies.

What is FDA's role regarding biological products?

FDA's regulatory authority for the approval of biologics resides in the Public Health Service Act (PHS). However, biologics are also subject to regulation under the Federal Food, Drug, and Cosmetic Act (FD&C Act) because most biological products also meet the definition of "drugs" cited within this Act.



BMY Webcast




Take Care,

Jimmy B

It's Time to Turn to Research's Most Valuable, Yet Underutilized Resource: Patients..Melanoma ..Jim Breitfeller

Thursday, August 27, 2009

It's Time to Turn to Research's Most Valuable, Yet Underutilized Resource: Patients

By Margaret Anderson, COO, FasterCures

It's Time to Turn to Research's Most Valuable, Yet Underutilized Resource: Patients


A piece in yesterday's New York Times, Research Trove: Patients' Online Data, recounts the story of a young woman stricken by a rare pulmonary disease, and her attempts to raise money and connect a network of scientists to research her ailment. In collaboration with a Harvard cancer researcher, she launched a Web site for others facing her same diagnosis, on which patients could share symptoms and report health information.

This kind of observational research, that focuses on empirical and experiential input, could prove invaluable in the quest to gain better understanding of disease and how it corrupts the functions of the human body. But there is more. Just as importantly, this story reinforces the contribution patients can make to their own medical care. In the search for cures, there is no substitute for patient engagement. For biomedical research to be effective and successful, it is imperative that it be patient driven. Empowering patients to play an active role in medical research requires transparent communication from trusted sources (i.e., frontline healthcare providers), a mechanism to ensure the patient's voice is heard loud and clear by decision and policy makers, the means for effective two-way communication between researchers and patients in real time, and informing the public about the value of clinical research to increase awareness and spur involvement.

FasterCures remains committed to supporting healthcare access but also in the creation of a “health cure” system that puts patients first.

So I contacted Frank Moss, director of the Massachusetts Institute of Technology Media Laboratory.

Dr. Moss, I read the piece on LAM and think this (Database) could also help Melanoma Cancer Patients. See I did a combination of clinical trials that jump started my immune system. I was told that I was a one off. Coming from a research background, I knew we are on to something big. So I researched my therapy. Here is the paper. Please if you got some time, take a look at it. Using the internet I was able to scientifically prove my theory.


Any Help would be greatly appreciated

Best regards


Response:

JIm,

Thanks for your note and very interesting paper. We are currently looking to expand the LAMsight approach to a more general platform that encompasses multiple diseases, perhaps melanoma could be included. Of course funding is an issue, but we are hopeful of cracking that nut in the near future. When we do we will get in touch.

Best,

Frank


________________________________
Frank Moss
Director of the Media Lab

MIT Media Lab
20 Ames Street, E15-401
Cambridge, MA 02139

Telephone: 617 324-3818
Fax: 617 253-8542


Take Care,

Jimmy B

Note to Bristol-Meyer Squibb,,Subject: TimeLine for compassionate drug use Ipilimumab.Melanoma.Jim Breitfeller

Subject: TimeLine for compassionate drug use Ipilimumab

It, has been over a year now that the compassionate drug use Ipilimumab was terminated due to production problems. As a chemist working in the field of biologics, I know it only takes about 3 months to generate Human Monoclonal antibodies. So why is it taking so long? I know you are trying different production protocols, but patients are loosing hope and their lives waiting for this drug. Will the compassionate use be reinstated soon? You say in your mission statement that:

“What sets us apart? We believe it's our commitment to patients with serious diseases, our focus on finding innovative medicines that combat those diseases, and our dedication to extending and enhancing human life.”

We need you Help Now!!!

Response:

Dear Mr. Breitfeller,

Thank you for your email.

As you are aware, Bristol-Myers Squibb and Medarex had to suspend enrollment of new patients into the compassionate use program and single patient exemptions to ensure treatment is not interrupted for patients currently receiving ipilimumab and to provide supply for ongoing clinical studies.

The manufacturing cycle time and testing of a biologic such as ipilimumab is complex. However, we are working through this process and continue to carefully manage the supply to enable the potential re-opening of compassionate use at the earliest possible time and when continuous supply is available. The companies recognize the great unmet medical need for patients with metastatic melanoma and remain committed to the development of ipilimumab.


Regards,


Bristol-Myers Squibb

Something doesn't seem right here. There is something going on. A year to get your Protocol in place that was already in place.

It doesn't smell right!!!!


I bet you it has something to do with the string of Pearls!!!!!!!!

Take Care,

Jimmy B

World first: Vaccine helps prevent HIV infection..Melanoma..Jim Breitfeller

World first: Vaccine helps prevent HIV infection

Two vaccines that did not work as a single agent, but combine them and they have 30% efficacy.

Read more: http://www.sfgate.com/cgi-bin/article.cgi?f=/n/a/2009/09/23/international/i224743D59.DTL&tsp=1#ixzz0S3Jo5WE0


What does HIV have to do with Melanoma?

HIV is an Immune System problem. It has to deal with your CD4+ T cells.

ARE YOU SEEING MY CORRELATION YET? We as Melanoma Patients need to activate our CD4+ T cells.

Interluekin-2 and Anti-CTLA-4 both have a low efficacy. But if you combine the two, with the right timing and dose, you will see synergistic results. The Final step is to get the right tumor specific antigen so the Cytotxic T- Cell can hone in on the tumors.

Here is an Email I just recieved:

"I asked my doc yesterday his opinion of your theory - IL2 + ipi = NED. He is in total agreement, and has seen it firsthand as well. He says he is actively pushing, but that he doesn't see it becoming available until next fall. AUGHHH!!!! So frustrating."

There is HOPE!!!!!!!




Take Care,

Jimmy B

A follow up with Dr. Paul Chapman and PLX4032 .. BRAF Mutation..Melanoma..Jim Breitfeller

Advancements in the treatment of metastatic malignant melanoma
23. September 2009 05:05

Researchers have made significant advances in the treatment of metastatic malignant melanoma - one of the most difficult cancers to treat successfully once it has started to spread - according to a study to be presented at Europe's largest cancer congress, ECCO 15 - ESMO 34, in Berlin on Thursday.

In the phase I extension study, researchers have seen rapid and dramatic shrinking of metastatic tumours in patients treated with a new compound that blocks the activity of the cancer-causing mutation of the BRAF gene, which is implicated in about 50% melanomas and 5% of colorectal cancers. In new results from 31 melanoma patients with the BRAF mutation who were treated with 960mg of PLX4032 twice a day, 64% (14) of the 22 patients who could be evaluated so far met the official criteria for partial response (this involves the diameter of tumours shrinking by at least 30% for at least a month). A further six of the 22 patients also showed a response, but, at the time of the congress presentation, it was too early to say whether the tumours would shrink far enough to meet these criteria.

Dr Paul Chapman, an attending physician on the Melanoma/Sarcoma service at Memorial Sloan-Kettering Cancer Center (New York, USA) and who was one of the leaders of the trial, told a news briefing: "We are very excited about these results. Of the 22 patients we have been able to evaluate so far, 20 have had some objective tumour shrinkage. This is impressive as they all had metastatic disease and most of them had failed several prior therapies. A lot of these patients were pretty sick but many of them had a significant and rapid improvement in the way they function. We've had patients come off oxygen and we've got several patients who have been able to come off narcotic pain medication soon after starting treatment."

The trial is investigating PLX4032 in patients with the BRAF mutation, and results from the first 55 patients were reported at a cancer meeting earlier this year (ASCO 2009). These data had been aimed at finding the best dose of PLX4032 to give to patients. However, the phase I extension data reported at ECCO 15 - ESMO 34 focuses on a subsequent group of an additional 31 patients who were all treated at the maximum tolerated dose of the drug (a 960 mg pill twice a day). All the patients had the BRAF mutation.

Dr Chapman said: "What makes this treatment different from standard chemotherapy is that standard chemotherapy attacks the machinery involved in cell division; so to stop the cancer cells dividing uncontrollably, most standard chemotherapy aims to block the mechanism of division by interfering directly with DNA replication or with microtubules in the dividing cells. PLX4302 is different because it attacks the genetic programme that is causing the cells to divide uncontrollably, and we think the BRAF mutation is driving that programme. The drug is blocking the genetics of the tumour, rather than trying to interfere with the proliferation of the cells and, as a result, there are fewer side effects, although there are some. We are seeing some pretty dramatic and rapid responses, and they are occurring in sites where we rarely see responses to chemotherapy, such as in the bone.

"There are some important caveats. All these patients had failed previous therapies, either chemotherapy or treatment with Interleukin 2, as well as surgery. However, we know that only 10-30% of patients will respond to standard chemotherapy, so it's not surprising that our patients had not responded, or have responded and then the cancer has recurred. In our study 64% of patients have had a partial response, but because we are only treating patients with the BRAF mutation, we are cutting out about 40% of melanoma patients who do not have this mutation and whom we know will not respond to this treatment. That is one reason why we are seeing a much higher response than with conventional treatments.

"Also, we don't know yet how long these responses will last, and we have had patients whose cancer has progressed after initially responding; so we are putting a lot of effort in to studying the patients who do relapse, trying to understand how their tumours have become resistant.

"In addition, one of the main side effects we've seen is that some patients develop early, non-melanoma skin cancers such as squamous cell skin cancer. We are very vigilant about this and although they are very easy to cut out, it's something we are keeping a close eye on."

Dr Chapman and his colleagues are planning a phase II trial of 90 patients starting at the end of this year. In addition, a large phase III randomised controlled trial involving several hundred patients is planned to start either at the end of this year or beginning of next year involving centres in North America, Europe and Australia.

Dr Chapman said it was too early to be talking about a cure for advanced melanoma, but that this drug had potential. "Most of us think that a drug like this would ultimately be part of the regimen, but that we might need additional drugs with it to complete the cure. Right now we are seeing dramatic responses but it's too early to say whether we've actually cured people because most patients still have evidence of some level of tumour on their skin. I think this is a huge step forward; whether or not it will be sufficient by itself really remains to be seen."

http://www.ecco-org.eu/Conferences-and-Events/ECCO-15/


You need to be genetically tested for the BRAF Mutation.



Take Care,

Jimmy B

How do you find a Specialist in Melanoma? Jim Breitfeller

Last Night I went to a Gilda Club Meeting on Melanoma. One Patient there asked "how do you find a specialist in Melanoma?" I believe whole heartedly that one must find the best team Leader to take you up Mount Everest. He/she is the only Clinical Oncologist that can guide you off the the Mountain. I could not recall this website, so I figured I would post it now.

www.melanomacare.org

Northeast:

Interdisciplinary Melanoma Program
Rhode Island Hospital
Brown Medical School
Providence, Rhode Island
401-444-8852
Michael P. Vezeridis, M.D.
Martin A. Weinstock, M.D., Ph.D.
Co-Directors

Melanoma Program
Norris Cotton Cancer Center
Dartmouth Hitchcock Medical Center
Lebanon, NH
603-650-5534

Skin Oncology Program
Boston Medical Center
Boston, MA
617-638-7131
Physician in charge: Marie-France Demierre, MD

The Melanoma Program at Massachusetts General Hospital
Pigmented Lesion Clinic, Arthur J. Sober, MD, Director
Surgical Oncology, Kenneth K. Tanabe, MD, Director
Medical Oncology, Frank G. Haluska, MD, PhD, Director
Boston, MA
617-724-6082

Pigmented Lesion Clinic
Beth Israel Deaconess Medical Center
Boston, MA
617-667-3753
physician in charge: Caroline C. Kim, MD

Pediatric Pigmented Lesion Clinic
Children's Hospital Boston
Boston, MA
617-355-6117
physician in charge: Caroline C. Kim, MD

Multidisciplinary Melanoma Clinic
University of Connecticut Health Center
Farmington, CT
860-679-4600

Pigmented Lesion Clinic
Yale Dermatology Consultants
New Haven, CT
203-785-4632

Roswell Park Cancer Institute
Buffalo, NY
716-845-7614

The Tumor Vaccine Program
Albert Einstein College of Medicine
New York, NY
718-430-2000

Melanoma Disease Management Team
Memorial Sloan-Kettering Cancer Center
New York, NY
212-610-0766
http://www.mskcc.org

Pigmented Lesion Section
New York University Medical Center, Oncology Section
New York, NY
212-263-5260
http://www.med.nyu.edu/derm

Comprehensive Cancer Center
Our Lady of Mercy Medical Center
New York, NY
718-920-1100

Mohs Micrographic and Dermatologic Surgery Unit
Department of Dermatology
Weill Medical College of Cornell
New York Presbyterian Hospital
New York, NY
212-746-6538

The Melanoma and Soft Tissue Oncology Program at
The Cancer Institute of New Jersey
UMDNJ-Robert Wood Johnson Medical School
New Brunswick, NJ
732-235-6777

Melanoma and Skin Cancer Program
University of Pittsburgh Cancer Institute
Hillman Cancer Center
Pittsburgh, PA
412-692-4724

Pigmented Lesion Group
Hospital of the University of Pennsylvania
Philadelphia, PA
215-662-6926

Midwest
Multidisciplinary Melanoma Clinic
Comprehensive Cancer Center, University of Michigan
Ann Arbor, MI
734-936-6360
http://www.cancer.med.umich.edu/clinic/melclinic.htm

Pigmented Lesion Clinic
Henry Ford Hospital
Detroit, MI
313-916-4060

Multidisciplinary Melanoma Clinic
Karmanos Cancer Institute
Wayne State University
Detroit, MI
313-745-9166
1-800-Karmanos

Multidisciplinary Melanoma and Pigmented Lesion Clinic
University of Cincinnati Medical Center
Cincinnati, OH
513-584-8900

MetroHealth Medical Center
Cancer Care Center Melanoma Program
2500 MetroHealth Drive
Cleveland, Ohio 44109

(216) 778-4795 (Surgical Oncology)
(216) 778-5802 (Medical Oncology)
The Melanoma Clinic at the Cleveland Clinic Taussig Cancer Center
Cleveland, OH
http://www.clevelandclinic.org/cancer

The Melanoma Center At The James
Ohio State University
Columbus, OH
614-293-7531 (medical)
614-293-5644 (surgical)

Wagner & Associates Plastic and Reconstructive Surgery Consultants of Indiana
Indianapolis, IN
317-621-2520
317-621-2580

Interdisciplinary Melanoma Clinic
Indiana University Cancer Center, Indiana University Medical Center
Indianapolis, IN
317-278-7449

Cardinal Bernardin Cancer Center
Loyola University Chicago
Chicago, IL
708-327-2078
http://www.luhs.org

Pigmented Lesion Center
Rush University
Chicago, IL
312-563-2321
http://www.rush.edu/rumc/page-R12605.html

Melanoma and Pigmented Lesion Center
University of Minnesota
Minneapolis, MN
612-625-5199

Multidisciplinary Melanoma Group
St. Louis University Health Sciences Center/SLUCare
St. Louis, MO
314-268-5320

South:

The Melanoma and Pigmented Lesion Clinic
Johns Hopkins Hospital
Baltimore, MD
410-614-1022

Melanoma Center
Washington Cancer Institute
The Washington Hospital Center
Washington, DC
202-877-2551
http://www.whc.mhg.edu

Blumenthal Cancer Center
Carolina Medical Center
Charlotte, NC
704-355-2757
http://www.carolinashealthcare.org

Dermatologic Surgery Unit, Department of Dermatology
Wake Forest University School of Medicine
Winston-Salem, NC
336-716-6276

The Melanoma Clinic/Pigmented Lesion Clinic
Duke Comprehensive Cancer Center
Durham, NC
919-684-2137

The University of North Carolina at Chapel Hill
Chapel Hill, NC 27514
Melanoma Multidisciplinary Program
Referrals/Appointments 919-966-9700

Brown Cancer Center, University Hospital at University of Louisville
Norton Cancer Center at Norton University
Louisville, KY
502-852-1897

The Dermatology Clinic
Vanderbilt University Medical Center
Nashville, TN
615-322-6485

Emory Surgery, Melanoma, and Pigmented Lesion Clinic
Emory University
Atlanta, GA
404-778-3354 (Dr Washington), 404-778-5225 (Dr Chen)

Section of Surgical Oncology
Winship Cancer Institute
Emory University
Atlanta, GA
Info: 404-778-5233

Oncology Research Program
Piedmont Hospital Research Institute
Atlanta, GA
404-605-3068
Email: phri@piedmont.org
http://www.piedmontcancercare.org

H. Lee Moffitt Cancer Center Cutaneous Oncology Clinic
Tampa, FL
813-972-8485
800-456-3434
813-972-8400 ext 1968 (new patients)
http://www.moffitt.usf.edu
Program Leader: Vernon K. Sondak, MD

Lakeland Regional Cancer Center
Cutaneous Oncology Program
Lakeland, FL
863-603-6565

The Pigmented Lesion Clinic
University of Miami School of Medicine
Miami, FL
305-243-4183

M. D. Anderson Cancer Center Orlando
1400 S. Orange Avenue
Orlando, Florida 32806
407 648-3800
800 648-3818
http://www.mdandersonorlando.org/

Melanoma Skin Center
Division of Internal Medicine, Department of Dermatology
M.D. Anderson Cancer Center
Houston, TX
713-745-1113

The Melanoma Center of North Texas
Dallas, TX
Phone: (214) 956-6802
Contact: Jody Jordan, CRA

West:

Melanoma Multidisciplinary Clinic
Huntsman Cancer Institute
Salt Lake City, UT
801-408-3555 (referrals)

Cutaneous Oncology
University of Colorado Cancer Center
Aschutz Cancer Pavilion
Aurora, CO
720-848-0300
800-473-2288

The Melanoma Center
UCSF Clinical Cancer Center
San Francisco, CA
415-885-7546

Northern California Melanoma Center
San Francisco, California
415-353-6535
Associate Director: Robert W. Weber, MD

Pigmented Lesion and Multidisciplinary Melanoma Clinics
Stanford University Medical Center
Stanford, CA
650-725-5255
http://cancer.stanfordhospital.com

The Angeles Clinic and Research Institute
Affiliated with the John Wayne Cancer Institute
Santa Monica, CA
310-231-2178
website: http://www.theangelesclinic.org/
email: info@theangelesclinic.org

The Pigmented Lesion Clinic
UCLA Dermatology Center
Los Angeles, CA
310-825-6911

North Bay Melanoma Program
Sponsored by Redwood Regional Medical Group
Director: Peter B. Brett, M.D.
652 Petaluma Ave #B
Sebastopol, CA 95472
website: http://www.melanomaprogram.org/
(707) 823-8565

CHAO Family Comprehensive Cancer Center-Melanoma Clinic
University of California, Irvine Medical Center
Orange, CA
714-456-8171

Seattle Cancer Care Alliance
University of Washington
Seattle, WA
206-288-2168 (patient referrals)

This is not the complete list, but a good starting point.

If patients around the world could add their center in the comments, I will add them to the on going list.

Thanks In advance



Take Care,

Jimmy B

Hope over new skin cancer therapy..Melanoma ..Jim Breitfeller

Hope over new skin cancer therapy

By Pallab Ghosh
Science correspondent, BBC News
Scientists have presented results of an experimental new drug which in early stage trials has significantly shrunk skin cancer tumours.

US rearchers from Memorial Sloan-Kettering Hospital in New York said their results were "unprecedented".

While not a cure, the study of 31 patients with late-stage skin cancer suggested the therapy could improve the quality of life and extend lifespan.

Larger scale trials will now be needed to test the drug, PLX4032, further.

In the study, which has been unveiled at a major cancer conference in Berlin, researchers treated patients where cancer had spread throughout their system.


We've seen responses in patients who didn't respond to chemotherapy before

Dr Paul Chapman, lead researcher
They were given a new drug that blocks the activity of a gene thought to be involved in the spread of skin cancer, the so-called BRAF gene.

Within two weeks they noticed what they described as a "rapid and dramatic" shrinking of the tumours in the cancer patients:

Lead researcher Dr Paul Chapman said: "We've seen responses in patients who didn't respond to chemotherapy before. So far 70 per cent of patients have responded. So that is unprecedented for us."

New treatments can often seem promising to begin with - but have disappointing results in later larger trials.

However, the doctors involved in the trial - and those at the European Cancer Organisation who have organised the conference - have never seen a cancer drug act so quickly on such a high proportion of patients.

SKIN CANCERS: THE FACTS



Skin cancers: In-depth UK data, symptoms, treatments and causes
The drug, PLX4032, is the latest in a new generation of cancer drugs that block the action of cancer causing genes.

The most successful of these so far has been Glivec (imatinib), which is used to treat myloid Leukaemia and gastric cancer.

Professor Alexander Eggermont, president of the European Cancer Organisation, said: "The new drug is the equivalent of Glivec in terms of the effect its having in advanced melanoma."

'It's fantastic'

One of those to receive the treatment was Mikhail Lvovsky, a dentist from New York.

A year ago he stopped work because he was so ill. He asked his doctor to take him off his previous medication because he could not bear the side effects. Now six months after taking the new drug he is back at work.

He said: "The first thing I did six months ago was to call the funeral director and pay for my funeral. Now I'm thinking of going back to work. It's beyond exciting. It's fantastic."

Dr Lvovsky's cancer is so serious it is unlikely for the new treatment to hold it back for very much longer longer.

But if the drug is shown to be effective in larger trials it has the potential to help people whose cancer is less advanced to live healthier and longer lives.

Alexander Eggermont, president of the European Cancer Organisation, described the trial as "simply spectacular".

He said it showed the benefits of targeting treatment.

The news would transform melanoma work into "a very exciting field instead of a graveyard", he said.

Dr Toby Chave, a consultant dermatologist at Derriford hospital in Plymouth, said: "Up to this point advanced melanoma has been extremely difficult to treat and does not respond well to any existing chemotherapy or radiotherapy.

"Prognosis is very poor. The new study shows that there is some response to the treatment which is very encouraging. Even giving patients the hope of a few extra months of life is significant for them."

However Dr Chave stressed that the new treatment was not a cure.

He added: "Any hope of long-term cure for advanced melanoma is still a long way off."

Hope over new skin cancer therapy

Source:http://news.bbc.co.uk/2/hi/health/8268719.stm
http://news.bbc.co.uk/1/hi/health/8269797.stm

Take Care,

Jimmy B

FDA Will Revisit Appropriate Use of PFS Endpoints at Advisory Committee..Melanoma..Jim Breitfeller

FDA Will Revisit Appropriate Use of PFS Endpoints at Advisory Committee

PFS= Pergression Free Survival

The Pink Sheet Daily. 2009 Sept 16, MJ Laffler

FDA Office of Oncology Drug Products Director Richard Pazdur plans to convene an advisory committee meeting to clarify standards for use of progression-free survival data, a move prompted by industry's aggressive adoption of the surrogate endpoint and, more broadly, the gradual decline in the level of drug benefit that sponsors seek to use in support of a cancer drug approval.

Though Pazdur wouldn't predict the timing of a meeting - beyond "soon" - he confirmed that it is an important issue that should be the topic of an upcoming meeting of the Oncologic Drugs Advisory Committee.

Industry Has Been Aggressive With PFS

In the last decade, there has been an extensive shift in oncology trials, with sponsors embracing the opportunity for earlier, arguably easier approval. The trend arose after FDA started accepting PFS as an early marker thought to be predictive of an eventual survival advantage - prompted by the urgent need for treatment options and availability of the accelerated approval pathway.

Allowing PFS to support accelerated approvals and eventually to support full approval did result in some impressive advances in medical oncology reaching patients years sooner than would have otherwise been possible. FDA has been careful to require trials to continue on in the post-market setting to demonstrate an overall survival finding, and the agency has upheld overall survival as the gold standard of efficacy evidence.

But the widespread reliance on PFS endpoints also created some sticky regulatory issues.

Source:FDA Will Revisit Appropriate Use of PFS Endpoints at Advisory Committee


As I see it, this PFS data can be used as a screening tool that shows that the drug/therapy has some response on the tumor regression/stabilization. It can be used as a predictive tool. The sooner we the patients can get our hands on the drug, the more lives may be saved. Take for instance tremelimumab and ipilimumab (Anti-CTLA-4 Blockage), it has shown great promise.

"At a meeting of cancer specialists last June Bristol-Myers and Medarex reported their drug shrank tumors in 46, or 13%, of 356 melanoma patients. The Pfizer antibody shrank melanomas in 7 of 84 patients in a midstage trial. The success rates were modest, but cancer doctors say that some patients may have had delayed responses. In some people tumors started to regress months after they had been declared treatment failures, says Bristol-Myers Vice President Renzo Canetta.

UCLA's Ribas calls the response rates "very low" and cautions that the anti-CTLA-4 drugs are just a first step. But even if the drugs improve survival only minimally, they are likely to be approved, he says.

One reason for the limited response rate may be that some patients' T cells do a poor job of recognizing melanoma. To improve this situation, researchers are combining new antimelanoma vaccines with anti-CTLA-4 drugs. The idea is that the vaccines will train T cells to spot cancer, while the antibody will make sure the T cells remain activated long enough to do their dirty work."

excerpts from FORBES.COM
Targeting Melanoma

author: Robert Langreth 10.15.07



Take Care,

Jimmy B

Search for a Cancer Vaccine Beginning to Show Promise..Melanoma ..Jim Breitfeller

Search for a Cancer Vaccine Beginning to Show Promise

As Reported by TIME. 2009 Sept 14

The search for an effective cancer vaccine has been elusive until now, but positive results for separate vaccines against melanoma and lymphoma were finally reported this past June. Although the theory behind a cancer vaccine seems logical—enlist the immune system to seek and destroy cancer cells—it also contains an inherent problem, specifically, that cancer cells aren’t foreign pathogens, such as bacteria or viruses, but cells from a person’s own body. Getting a vaccine to work against cancer requires a deep understanding of how the immune system works and how malignant cells evade detection. A feature article in the September 14 issue of TIME, written by Alice Park, explains the quest thus far for cancer vaccines.

Defining a cancer vaccine

The Food and Drug Administration has approved vaccines against cervical cancer and liver cancer, but both of these diseases are caused by a virus (human papillomavirus and hepatitis B virus, respectively). Thus, the vaccines are actually targeting the virus. Nonviral cancers attributed to genetic mutations, environmental exposures, and other factors would require a vaccine that can accomplish primary prevention or prevention of recurrence. Such vaccines would need to prime the immune system to find every last cancer cell.

Cancer vaccines that didn’t work, but might

A vaccine for melanoma seemed on the horizon when researchers used extracts of melanoma tumors in developing Canvaxin. More than 1500 patients received the vaccine following treatment with surgery and chemotherapy, but the study was terminated after interim analysis showed that survival was no better for the vaccinated patients than for the nonvaccinated patients. Addition of interleukin-2, however, improved the rate of tumor shrinkage. Researchers working on a vaccine for follicular lymphoma took the combination approach one step further, by adding GM-CSF to a vaccine developed from each patient’s cancer cells. This combination extended disease-free survival by 47% over that achieved by patients who received a nonindividualized vaccine. Experience with this vaccine also indicated that the best time to administer the vaccine was when patients were in remission.

Creating a “foreign” tumor

Various strategies to manipulate a tumor to cause it to become more “foreign” are being investigated. One technique is to make the tumor look like a virus to the immune system. Another is to inhibit immune suppressors that tumors secrete. Along the lines of the bone marrow transplantation approach, some studies have used in vitro techniques to develop immune system cells, taken from the cancer patient, that will target those specific cancer cells; the newly sensitized immune cells are then reinfused back into the patient. In melanoma, this approach has caused 70% of tumors to regress.

The final analysis

Regardless of how effectively a vaccine causes tumor regression, patients and their physicians are most interested in its effect on survival. Also important is how use of a vaccine compares with the targeted therapies that have been developed. For cancer to become a truly chronic condition, manageable over the long term, a vaccine or treatment must be safe. Vaccines, as it turns out, are generally less toxic than chemotherapy or targeted agents. Immune-based treatments for cancer are still in their infancy, but if they are ultimately proven successful, their development would be well worth the effort.

Source:http://www.oncologystat.com/news-and-viewpoints/what_patients_are_reading/Search_for_a_Cancer_Vaccine_Beginning_to_Show_Promise.html

My take:Creating a “foreign” tumor

If you can get the tumor to shed antigenic peptide and then activate the T-cells using anti-CTLA-4 Blockage, I believe you will see the Melanoma survival rate expand and that Melanoma will become just a "chronic condition,manageable over the long term."






Take Care,

Jimmy B

Inherent Complexities in Melanoma Research..Jim Breitfeller

Inherent Complexities in Melanoma Research

NCI Conference Highlights Promising Advances in Immunotherapy
EASTMAN, PEGGY

Oncology Times:
25 October 2008 - Volume 30 - Issue 20 - p 32-35


Still challenging researchers and slowing progress in the field of cancer immunology and immunotherapy are the inherent complexities of immunity, said other speakers at the meeting.
Regulation of T-cell responses is a lot more complex than we had initially thought, noted James P. Allison, PhD, Director of the Ludwig Center of Cancer Immunotherapy and Chairman of the Immunology Program at Memorial Sloan-Kettering Cancer Center.


Dr. Allison said that one reason there have not been more successful clinical strategies to mobilize the immune system to attack cancer cells is that until recently not enough attention has been paid to the multiple inhibitory mechanisms that serve to shape the immune response and minimize harm to normal tissues.

These mechanisms, he said, are a collective obstacle that can frustrate generation of effective anti-tumor responses.
His research has shown that the prototype of these inhibitory pathways is CTLA4, which limits T-cell proliferation. We have shown that blockade of CTLA4 can greatly enhance anti-tumor responses in a number of experimental tumors in mice, he said, noting that the CTLA4 blocker ipilimumab is now being developed by Medarex, Inc., and Bristol-Myers Squibb.

The results of clinical trials in more than 3,500 patients [for ipilimumab] have demonstrated objective, durable responses in a subset of melanoma, renal, ovarian, and prostate cancer patients. Thus for the first time we have objective responders, which he called exciting.

James C. Yang, MD, Senior Investigator in NCI's Surgery Branch, said that one immunotherapy combination of special clinical interest is ipilimumab plus interleukin-2 (IL-2). Dr. Yang, who chaired a symposium session, noted that in a Phase I/II study of 36 melanoma patients who received dose-escalating ipilimumab with a high-dose bolus of IL-2, the overall response rate was 22%. Long-term follow-up shows that six of the eight responders achieved ongoing complete responses with durations all exceeding four years.


Anti-CTLA4 antibodies have also been tried with other cancers, said Dr. Yang. He added that to extend the role of anti-CTLA4 therapy to a broader array of cancers, it will likely be necessary to combine it with other immunological manipulations, a combination approach which will hopefully boost the host immune response to cancer.


Take Care,

Jimmy B

Experimental Vaccine Improves Response in Melanoma!!!..Jim Breitfeller

Laino, Charlene
Oncology Times:
25 August 2009 - Volume 31 - Issue 16 - pp 39-41
doi: 10.1097/01.COT.0000360410.38201.57


ORLANDO, FL-For the first time, a synthetic peptide vaccine designed to boost immunogenicity has been shown to improve outcomes in patients with metastatic melanoma in a Phase III clinical trial.
Used in conjunction with standard interlekin-2 (IL-2) therapy, the vaccine improved the clinical response rate and prolonged the time to disease progression, compared with IL-2 alone, Patrick Hwu, MD, Professor and Chairman of the Department of Melanoma Medical Oncology at the University of Texas M. D. Anderson Cancer Center, reported here at the ASCO Annual Meeting.

There was also a trend toward improved survival rates among patients given the vaccine, but the patients have to be followed longer before we can see statistical significance, he said.

'A Nice Milestone'

The so-called gp100:209-217(210M) peptide vaccine is a synthetic peptide cancer vaccine consisting of amino acid residues 209 through 217 of the glycoprotein 100 (gp100) melanoma antigen, with a methionine substitution at position 210 designed to improve immunogenicity. It's given along with IL-2, a powerful immune-system stimulant.


Vaccination with gp100:209-217 (210M) peptide stimulates the patient's immune system to mount a cytotoxic T-lymphocyte response against tumor cells expressing gp100, Dr. Hwu explained. The IL-2 multiplies the T cells into a large army that can then attack the tumors to kill them.
In a Phase II trial led by Steven Rosenberg, MD, PhD, 42% of 31 patients with metastatic melanoma receiving high-dose IL-2 plus the vaccine had objective responses, but this is the first Phase III study of the vaccine that is positive, Dr. Hwu said. It's a nice milestone.

21-Center Study

The 21-center, Phase III trial involved 185 patients with Stage IV or locally advanced Stage III cutaneous metastatic melanoma, randomized to receive either the peptide vaccine followed by four days of high-dose IL-2 at 720,000 IU/kg/dose or high-dose IL-2 alone. The cycle was repeated every three weeks until the patients responded or progressed.
The overall clinical response rate was almost double in the vaccine arm-22.1%, compared with 9.7% for the patients who got interleukin-2 alone, Dr. Hwu said.

The median progression-free survival time was 2.9 months in the vaccine arm vs 1.6 months for IL-2 alone, again a significant difference.
The median overall survival time was 17.6 months in the vaccine arm compared with 12.8 in the IL-2 alone arm, but the difference did not reach statistical significance, Dr. Hwu said.

The vaccine was well tolerated. Side effects were swelling and redness at the injection site.

'Rare, Positive Study in Metastatic Melanoma'

This is a rare positive study in metastatic melanoma, said the Discussant, Antoni Ribas, MD, Associate Professor of Medicine (Hematology/Oncology) and Surgery (Surgical Oncology) at UCLA.
Dr. Ribas said he would like to see further study to determine if the vaccine prolongs overall survival times. But since accruement for the current study took seven years, it's uncertain that anyone will want to undertake a confirmatory Phase III trial for overall survival, he said.
Louis M. Weiner, MD, Director of the Lombardi Comprehensive Cancer Center, said he views this as a conceptual advance, teaching us that focusing the attention of the immune system on a specific cancer-related target increases the ability of the immune system to attack tumors, at least for a while.

Many of us believe that a combined approach that includes an immune system attack on cancer cells will ultimately prove to be most useful in controlling cancers such as melanoma, he said.
Dr. Weiner said one reason this vaccine may have worked while others have failed is because it was combined with high-dose IL-2.



We have known for a while that IL-2 therapy is effective in a small percentage of melanoma patients. But when it is effective, it is highly effective, he said.

But IL-2 can be toxic and is not simple to use, Dr. Weiner said.
The moderator of a news conference at the meeting that featured the study, Sonali M. Smith, MD, Associate Professor of Medicine at the University of Chicago Medical Center, called the findings very promising for a very poor-prognosis group of patients, and said that the approach might act as a platform for more potent vaccines.
Dr. Hwu agreed, noting that 80% of patients did not respond. He said he hopes to improve response rates in future trials by combining the vaccine with other immune-stimulating agents such as anti-CTLA-4.

Cytotoxic T lymphocyte antigen 4 (CTLA-4), a key negative regulator of T-cell responses, can restrict the antitumor immune response. By using an anti-CTLA-4 agent, he said, we can take the brakes off the immune system, which should allow the vaccine and IL-2 to work even better.

Source:http://journals.lww.com/oncology-times/Fulltext/2009/08250/Experimental_Vaccine_Improves_Response_in_Melanoma.15.aspx

I believe this aproach will show tremendous progress in Melanoma Therapy






Take Care,

Jimmy B

As I Continue my Quest, I have come to another Windmill..Melanoma..Jim Breitfeller

As I Continue my Quest, I have come to another Windmill.

Anti-CTLA-4 Blockage maybe coming back to compassionate care or better yet,may be getting ready to seek FDA approval.

I have stumble upon another Review Article by Dr. Kim Margolin from 2008.

"Moving forward with immunotherapy: the rationale for anti-CTLA-4 therapy in melanoma."

Source:http://www.communityoncology.net/journal/articles/0507367.pdf
Moving forward with immunotherapy: the rationale for anti-CTLA-4 therapy in melanoma

If you look closely at the tables, you know why Brisol-Meyer Squibb aquired Medarex for their "String of Pearls".

This is the quote I like the Best:

"The preliminary results of these trials are encouraging, considering most patients were previously treated for advanced melanoma. The possibility that anti-CTLA-4 antibodies, used as single agents, will be superior to proven therapies, ie, dacarbazine or IL-2, will be tested in phase III trials. Of greater promise may be the combination of these agents in carefully timed sequence with cytotoxic or other immunotherapeutic strategies."

See , I believe that the combination therapies Hold the greatest Promise.
I can vouch for that. NED FOR OVER 25 MONTHS AND STILL COUNTING!!!!!

Please seek out this therapy if you need it. It could extend or even save your life.



Take Care,

Jimmy B