Genentech has just opened a study for people who have taken the Plexxikon/Roche/Genentech BRAF inhibitor, also known as PLX 4032. This study is a combination trial using PLX plus a MEK inhibitor. Some folks from this board have been in the BRAF/MEK trial being run by GSK, and this new trial is similar. One criteria, though, is that you must have taken the Plexxikon drug and have developed resistance to that drug. Currently three sites are open: Dr. Gajewski in Chicago, Dr. Ribas in UCLA, and Dr. Gonzalez in Denver. Four more sites will open soon. You can go to this link to find out information about melanoma relevant clinical trials, including this one: http://www.emergingmed.com/networks/MRF
Source: Tim--MRF
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
This is Jim Breitfeller's journey into the Maze of Melanoma. Jim Breitfeller has gathered medical information for the patient and the caregiver. As Lance Armstrong would say "Lets stand Up to Cancer" Jim's Battle with the Beast July 2005 to present.
Tuesday, March 29, 2011
Saturday, March 26, 2011
Profitable are the sick, for they shall be exploited..Melanoma..BMS ..Jim Breitfeller
Profitable are the sick, for they shall be exploited
I know many Melanoma Patients turned away by Bristol Myer Squibb.
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
I know many Melanoma Patients turned away by Bristol Myer Squibb.
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Friday, March 25, 2011
F.D.A. Approves Drug to Treat Melanoma..Jim Breitfeller
The FDA just announced that they have approved Yervoy "ipi" for unresectable and metastatic melanoma. This is the first time a drug has been approved for melanoma in 13 years, so great news!
Here's the announcement:
FDA NEWS RELEASE
For Immediate Release: March 25, 2011
Media Inquiries: Erica Jefferson, 301-796-4988, erica.jefferson@fda.hhs.gov
Consumer Inquiries: 888-INFO-FDA
FDA approves new treatment for a type of late-stage skin cancer
Melanoma patients lived longer with treatment
The U.S. Food and Drug Administration today approved Yervoy (ipilimumab) to treat patients with late-stage (metastatic) melanoma, the most dangerous type of skin cancer.
Melanoma is the leading cause of death from skin disease. An estimated 68,130 new cases of melanoma were diagnosed in the United States during 2010 and about 8,700 people died from the disease, according to the National Cancer Institute.
"Late-stage melanoma is devastating, with very few treatment options for patients, none of which previously prolonged a patient's life," said Richard Pazdur, M.D., director of the Office of Oncology Drug Products in the FDA's Center for Drug Evaluation and Research. "Yervoy is the first therapy approved by the FDA to clearly demonstrate that patients with metastatic melanoma live longer by taking this treatment."
Yervoy is a monoclonal antibody that blocks a molecule known as cytotoxic T-lymphocyte antigen or CTLA-4. CTLA-4 may play a role in slowing down or turning off the body's immune system, affecting its ability to fight off cancerous cells. Yervoy may work by allowing the body's immune system to recognize, target, and attack cells in melanoma tumors. The drug is administered intravenously.
Yervoy's safety and effectiveness were established in a single international study of 676 patients with melanoma. All patients in the study had stopped responding to other FDA-approved or commonly used treatments for melanoma. In addition, participants had disease that had spread or that could not be surgically removed.
The study was designed to measure overall survival, the length of time from when this treatment started until a patient's death. The randomly assigned patients received Yervoy plus an experimental tumor vaccine called gp100, Yervoy alone, or the vaccine alone.
Those who received the combination of Yervoy plus the vaccine or Yervoy alone lived an average of about 10 months, while those who received only the experimental vaccine lived an average of 6.5 months.
Common side effects that can result from autoimmune reactions associated with Yervoy use include fatigue, diarrhea, skin rash, endocrine deficiencies (gland or hormone), and inflammation of the intestines (colitis). Severe to fatal autoimmune reactions were seen in 12.9 percent of patients treated with Yervoy.When severe side effects occurred, Yervoy was stopped and corticosteroid treatment was started. Not all patients responded to this treatment. Patients who did respond in some cases did not see any improvement for several weeks.
Due to the unusual and severe side effects associated with Yervoy, the therapy is being approved with a Risk Evaluation and Mitigation Strategy to inform health care professionals about these serious risks. A medication guide will also be provided to patients to inform them about the therapy's potential side effects.
Yervoy is marketed by New York City-based Bristol-Myers Squibb.
For more information:
FDA: Office of Oncology Drug Products
http://www.fda.gov/AboutFDA/CentersOffices/CDER/ucm091745.htm
FDA: Approved Risk Evaluation and Mitigation Strategies (REMS)
http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm111350.htm
FDA: Approved Drugs: Questions and Answers
http://www.fda.gov/Drugs/ResourcesForYou/Consumers/ucm054420.htm
NCI: Melanoma
http://www.cancer.gov/cancertopics/types/melanoma
CDC: Skin Cancer
http://www.cdc.gov/cancer/skin/
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Here's the announcement:
FDA NEWS RELEASE
For Immediate Release: March 25, 2011
Media Inquiries: Erica Jefferson, 301-796-4988, erica.jefferson@fda.hhs.gov
Consumer Inquiries: 888-INFO-FDA
FDA approves new treatment for a type of late-stage skin cancer
Melanoma patients lived longer with treatment
The U.S. Food and Drug Administration today approved Yervoy (ipilimumab) to treat patients with late-stage (metastatic) melanoma, the most dangerous type of skin cancer.
Melanoma is the leading cause of death from skin disease. An estimated 68,130 new cases of melanoma were diagnosed in the United States during 2010 and about 8,700 people died from the disease, according to the National Cancer Institute.
"Late-stage melanoma is devastating, with very few treatment options for patients, none of which previously prolonged a patient's life," said Richard Pazdur, M.D., director of the Office of Oncology Drug Products in the FDA's Center for Drug Evaluation and Research. "Yervoy is the first therapy approved by the FDA to clearly demonstrate that patients with metastatic melanoma live longer by taking this treatment."
Yervoy is a monoclonal antibody that blocks a molecule known as cytotoxic T-lymphocyte antigen or CTLA-4. CTLA-4 may play a role in slowing down or turning off the body's immune system, affecting its ability to fight off cancerous cells. Yervoy may work by allowing the body's immune system to recognize, target, and attack cells in melanoma tumors. The drug is administered intravenously.
Yervoy's safety and effectiveness were established in a single international study of 676 patients with melanoma. All patients in the study had stopped responding to other FDA-approved or commonly used treatments for melanoma. In addition, participants had disease that had spread or that could not be surgically removed.
The study was designed to measure overall survival, the length of time from when this treatment started until a patient's death. The randomly assigned patients received Yervoy plus an experimental tumor vaccine called gp100, Yervoy alone, or the vaccine alone.
Those who received the combination of Yervoy plus the vaccine or Yervoy alone lived an average of about 10 months, while those who received only the experimental vaccine lived an average of 6.5 months.
Common side effects that can result from autoimmune reactions associated with Yervoy use include fatigue, diarrhea, skin rash, endocrine deficiencies (gland or hormone), and inflammation of the intestines (colitis). Severe to fatal autoimmune reactions were seen in 12.9 percent of patients treated with Yervoy.When severe side effects occurred, Yervoy was stopped and corticosteroid treatment was started. Not all patients responded to this treatment. Patients who did respond in some cases did not see any improvement for several weeks.
Due to the unusual and severe side effects associated with Yervoy, the therapy is being approved with a Risk Evaluation and Mitigation Strategy to inform health care professionals about these serious risks. A medication guide will also be provided to patients to inform them about the therapy's potential side effects.
Yervoy is marketed by New York City-based Bristol-Myers Squibb.
For more information:
FDA: Office of Oncology Drug Products
http://www.fda.gov/AboutFDA/CentersOffices/CDER/ucm091745.htm
FDA: Approved Risk Evaluation and Mitigation Strategies (REMS)
http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm111350.htm
FDA: Approved Drugs: Questions and Answers
http://www.fda.gov/Drugs/ResourcesForYou/Consumers/ucm054420.htm
NCI: Melanoma
http://www.cancer.gov/cancertopics/types/melanoma
CDC: Skin Cancer
http://www.cdc.gov/cancer/skin/
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Thursday, March 24, 2011
Late-Breaking Abstracts..Melanoma ..Jim Breitfeller
Late-Breaking Abstracts
2010 Annual Meeting; Washington, D.C., October 2-4, 2010 3
International Society for Biological Therapy of Cancer (iSBTc; now known as the Society for Immunotherapy of Cancer; SITC)
-162-
USING TIMING TO SYNCHRONISE IMMUNOTHERAPY THROUGH
MICROMANIPULATION OF THE UNDERLYING TUMOR IMMUNE RESPONSE:
FROM COLEY TO ROSENBERG, LOTZE, ALLISON, WOLCHOK AND BEYOND!
Brendon J. Coventry1, Martin L. Ashdown2, Svetomir N. Markovic3
1Surgery and Immunology, University of Adelaide, Adelaide, SA, Australia
2Medicine, University of Melbourne, Melbourne, VIC, Australia
3Medical Oncology, Mayo Clinic, Rochester, MN
Introduction: Immunotherapy studies in advanced cancers appear to show that the immune
response can be driven in either an ‘effector’ or ‘regulatory’ direction or a ‘mixture’ of these,
leading to the heterogeneous clinical responses (CR, PR, PD) seen. Using CRP as a marker, we
have shown that a repeating cyclical, dependent, sequential, orchestrated, homeostatic
physiologic process appears to be occurring in most, if not all, cancer patients, most likely as a
result of chronic antigenic stimulation. The correct timing of immunotherapy or chemotherapy
with this ‘immune cycle’ appears to be associated with better cancer control and improved
clinical outcomes.
We are concerned that the timing of therapy with respect to the underlying tumor immune
response fluctuations is the principal determinant of efficacy in cancer treatment. The
observations and model may also extend to other chronic inflammatory states to determine
therapeutic efficacy.
Methods: Using serial CRP measurements in late-stage cancer patients, we have recently been
able to expose sequential and time dependent oscillations in the inflammatory/ immune response
that may represent a homeostatic, repeating or cyclical process of tumour immune
responsiveness then tolerance. The periodicity of these cycles appears to be reproducible at
approximately 6-7 days.
By serially measuring CRP around the time of vaccination or chemotherapy, the position on the
underlying immune curve can be established. Timing with respect to this cycle appears to be
critical to modulating the immune system with each intervention, and pivotal to the clinical
efficacy of therapy (1,2).
Results: Using these methods, we have been able to correlate the timing of vaccination/
chemotherapy with the induction of clinical responses. Induction of complete responses, stable
disease, slowed growth even with persistent metastatic disease, appears possible using these
principles, thereby improving overall survival.
Conclusions: The historical ‘random successes’ seen with vaccines, cytokines and receptor
directed monoclonal antibodies may be due to their fortuitous accidental interference with the
underlying persistent, homeostatically regulated tumor immune kinetics by their ‘random’
untimed administration. By accurately and appropriately synchronizing therapy to each patient’s
immune system’s periodic oscillations - immune cycle - we predict that the current low random
immunotherapy successes seen to date, can be made more predictable by accurately timing
therapy better, and will achieve greater clinical efficacy.
Where have you heard the key to an immune response is dose and timming.
Right Here
Melanoma and the Magic Bullet
The Research paper called Melanoma and the Magic Bullet
The Research paper called The Making of an Immune Response by Combinatorial Therapy Using Anti-CTLA-4 Blockade and Interleukin-2
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
2010 Annual Meeting; Washington, D.C., October 2-4, 2010 3
International Society for Biological Therapy of Cancer (iSBTc; now known as the Society for Immunotherapy of Cancer; SITC)
-162-
USING TIMING TO SYNCHRONISE IMMUNOTHERAPY THROUGH
MICROMANIPULATION OF THE UNDERLYING TUMOR IMMUNE RESPONSE:
FROM COLEY TO ROSENBERG, LOTZE, ALLISON, WOLCHOK AND BEYOND!
Brendon J. Coventry1, Martin L. Ashdown2, Svetomir N. Markovic3
1Surgery and Immunology, University of Adelaide, Adelaide, SA, Australia
2Medicine, University of Melbourne, Melbourne, VIC, Australia
3Medical Oncology, Mayo Clinic, Rochester, MN
Introduction: Immunotherapy studies in advanced cancers appear to show that the immune
response can be driven in either an ‘effector’ or ‘regulatory’ direction or a ‘mixture’ of these,
leading to the heterogeneous clinical responses (CR, PR, PD) seen. Using CRP as a marker, we
have shown that a repeating cyclical, dependent, sequential, orchestrated, homeostatic
physiologic process appears to be occurring in most, if not all, cancer patients, most likely as a
result of chronic antigenic stimulation. The correct timing of immunotherapy or chemotherapy
with this ‘immune cycle’ appears to be associated with better cancer control and improved
clinical outcomes.
We are concerned that the timing of therapy with respect to the underlying tumor immune
response fluctuations is the principal determinant of efficacy in cancer treatment. The
observations and model may also extend to other chronic inflammatory states to determine
therapeutic efficacy.
Methods: Using serial CRP measurements in late-stage cancer patients, we have recently been
able to expose sequential and time dependent oscillations in the inflammatory/ immune response
that may represent a homeostatic, repeating or cyclical process of tumour immune
responsiveness then tolerance. The periodicity of these cycles appears to be reproducible at
approximately 6-7 days.
By serially measuring CRP around the time of vaccination or chemotherapy, the position on the
underlying immune curve can be established. Timing with respect to this cycle appears to be
critical to modulating the immune system with each intervention, and pivotal to the clinical
efficacy of therapy (1,2).
Results: Using these methods, we have been able to correlate the timing of vaccination/
chemotherapy with the induction of clinical responses. Induction of complete responses, stable
disease, slowed growth even with persistent metastatic disease, appears possible using these
principles, thereby improving overall survival.
Conclusions: The historical ‘random successes’ seen with vaccines, cytokines and receptor
directed monoclonal antibodies may be due to their fortuitous accidental interference with the
underlying persistent, homeostatically regulated tumor immune kinetics by their ‘random’
untimed administration. By accurately and appropriately synchronizing therapy to each patient’s
immune system’s periodic oscillations - immune cycle - we predict that the current low random
immunotherapy successes seen to date, can be made more predictable by accurately timing
therapy better, and will achieve greater clinical efficacy.
Where have you heard the key to an immune response is dose and timming.
Right Here
Melanoma and the Magic Bullet
The Research paper called Melanoma and the Magic Bullet
The Research paper called The Making of an Immune Response by Combinatorial Therapy Using Anti-CTLA-4 Blockade and Interleukin-2
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Tuesday, March 22, 2011
Bristol-Myers Awaits Approval for Drug's New Cancer Attack
With This FDA Approval, This is the begining of the end cancer as we know it. Ipilimumab will revolutionize Cancer therapy along with Anti-PD-1 and HD IL-2.
Bristol-Myers Awaits Approval for Drug's New Cancer Attack
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Bristol-Myers Awaits Approval for Drug's New Cancer Attack
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Thursday, March 17, 2011
Sounding the Danger Signal through chemotherapy to Cause Cancer Cell Death..Melanoma ..Jim Breitfeller
Sounding the Danger Signal through chemotherapy to Cause Cancer Cell Death
“Schedule and Dose for Combination Therapy,”
2011 Scientific Colloquium of the Cancer Immunotherapy Consortium
Thursday, March 17, 2011 7:00 AM - Saturday, March 19, 2011 1:30 PM
Eastern Time
Dr. Hy Levitsky is introducing Dr. Laurence Zitvogel from Institut Gustave Roussy, a leader in cell biology in cancer.
New Speaker: Laurence Zitvogel, Ph.D.
Institut GustaveRoussy, Villejuif, France
"Dr. Zitvogel graduated in medical oncology from the School of Medicine of the University of Paris in 1992. She started her scientific career when she was at the University of Pittsburgh in Michael Lotze’s laboratory. She became research director at Institut National de la Santé et Recherche Médicale in a laboratory located at Institut Gustave Roussy, a large cancer center in Villejuif, France, and the head of the Center for Clinical Investigations for vaccine developments at Villejuif. Dr. Zitvogel has been actively contributing to the field of cancer immunology and immunotherapy, bringing together basic and translational research, including the design of cancer therapies through combined animal studies and phase I patient trials. Her expertise is mainly dendritic cell and innate effector biology and relevance during tumor development, as well as exosome-based vaccine designs."
Zitvogel: chemotherapy may work because cancer cell death is immunogenic and triggers anti-cancer immunity
Zitvogel: Chemo causes cancer to express "eat me" or "come and get me" signals to the immune system. Nice way to phrase it!
Jimmy B: See Graph Below
Autophagy Defintion: The process of self-digestion by a cell through the action of enzymes originating within the same cell.
Zitvogel: "autophagy" is important to death of cancer cells. It breaks down in cancer growth. Chemo re-starts the autophagy process.
Zitvogel: some types of chemo are better at inducing immunogenic cell death than others. Cisplatin and taxols aren't strong in this.
Zitvogel: new tests can show how a drug falls short in triggering immunogenic cancer death -- and how to compensate for that.
Zitvogel: Giving thapsigarin can improve cisplatin's ability to trigger immunogenic cancer cell death.
Jimmy B: Thapsigargin sensitizes human melanoma cells to TRAIL-induced apoptosis
Zitvogel: "drug repositioning" is the process of combining drugs to compensate for where one falls short in immunogenic cell death.
Zitvogel: combining immunogenic chemotherapies with immunomodulators or other immunotherapy is a very promising strategy.
Source: Cancer Research on Twitter
http://twitter.com/#!/search?q=%23cic11
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
“Schedule and Dose for Combination Therapy,”
2011 Scientific Colloquium of the Cancer Immunotherapy Consortium
Thursday, March 17, 2011 7:00 AM - Saturday, March 19, 2011 1:30 PM
Eastern Time
Dr. Hy Levitsky is introducing Dr. Laurence Zitvogel from Institut Gustave Roussy, a leader in cell biology in cancer.
New Speaker: Laurence Zitvogel, Ph.D.
Institut GustaveRoussy, Villejuif, France
"Dr. Zitvogel graduated in medical oncology from the School of Medicine of the University of Paris in 1992. She started her scientific career when she was at the University of Pittsburgh in Michael Lotze’s laboratory. She became research director at Institut National de la Santé et Recherche Médicale in a laboratory located at Institut Gustave Roussy, a large cancer center in Villejuif, France, and the head of the Center for Clinical Investigations for vaccine developments at Villejuif. Dr. Zitvogel has been actively contributing to the field of cancer immunology and immunotherapy, bringing together basic and translational research, including the design of cancer therapies through combined animal studies and phase I patient trials. Her expertise is mainly dendritic cell and innate effector biology and relevance during tumor development, as well as exosome-based vaccine designs."
Zitvogel: chemotherapy may work because cancer cell death is immunogenic and triggers anti-cancer immunity
Zitvogel: Chemo causes cancer to express "eat me" or "come and get me" signals to the immune system. Nice way to phrase it!
Jimmy B: See Graph Below
Autophagy Defintion: The process of self-digestion by a cell through the action of enzymes originating within the same cell.
Zitvogel: "autophagy" is important to death of cancer cells. It breaks down in cancer growth. Chemo re-starts the autophagy process.
Zitvogel: some types of chemo are better at inducing immunogenic cell death than others. Cisplatin and taxols aren't strong in this.
Zitvogel: new tests can show how a drug falls short in triggering immunogenic cancer death -- and how to compensate for that.
Zitvogel: Giving thapsigarin can improve cisplatin's ability to trigger immunogenic cancer cell death.
Jimmy B: Thapsigargin sensitizes human melanoma cells to TRAIL-induced apoptosis
Zitvogel: "drug repositioning" is the process of combining drugs to compensate for where one falls short in immunogenic cell death.
Zitvogel: combining immunogenic chemotherapies with immunomodulators or other immunotherapy is a very promising strategy.
Source: Cancer Research on Twitter
http://twitter.com/#!/search?q=%23cic11
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
“Schedule and Dose for Combination Therapy,” Melanoma.. 2011 Scientific Colloquium of the Cancer Immunotherapy
“Schedule and Dose for Combination Therapy,”
2011 Scientific Colloquium of the Cancer Immunotherapy Consortium
• Thursday, March 17, 2011 7:00 AM - Saturday, March 19, 2011 1:30 PM
Eastern Time
First Speaker: Dr. Rafi Ahmed
Director of the Emory Vaccine Center
"As a basic immunologist, EVC Director Dr. Rafi Ahmed studies immunological memory – the ability of the immune system to “remember” a particular antigen and respond accordingly. Dr. Ahmed and his colleagues have made significant discoveries about how immune memory cells are created and how long they survive; understanding these mechanisms is crucial to the development of vaccines for HIV and other infectious agents. In addition to contributing vitally to vaccine science, Dr. Ahmed’s findings are being applied to research into therapies for the treatment of cancer and the prevention of organ rejection."
Dr. Rafi Ahmed is now being introduced by Johannes Vieweg, & highlighting his work on immunological memory
Dr. Ahmed is sharing how lessons from immune memory development in chronic viral infection can inform cancer immunotherapy field
Ahmed: wait 30-60 days to boost in vaccination produces better immune responses for many types of viral vaccines. Same for cancer?JimmyB :Why 30 to 60 days? Because this is the time factor that it takes for the CD4+ and CD8+ T-cells to grow and differentiate into effector T-cells. (See Graph)
Fig-1
Dr. Rafi Ahmed is now being introduced by Johannes Vieweg, & highlighting his work on immunological memory Dr. Ahmed is sharing how lessons from immune memory development in chronic viral infection can inform cancer immunotherapy field Ahmed: wait 30-60 days to boost in vaccination produces better immune responses for many types of viral vaccines. Same for cancer?
Fig-2
Ahmed: Synergy we've seen combining PD-1 with IL-2 (negative + positive signal) in viral infection therapy have been astonishing.
Jimmy B:Imagine if you combine CTLA-4 + PD-1 and IL-2. The Holy Grail of Immuno therapy I believe.Ahmed raises point that mTOR inhibition may enhance vaccine-induced memory CD8 T-cells. Role for combining with cancer vaccines?
Much audience Q&A for Dr. Ahmed - when see exhaustion clinically, is it inhibition, effect of dose of IL-2, and role of autophagy?
Source: Cancer Research on Twitter
http://twitter.com/#!/search?q=%23cic11
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
2011 Scientific Colloquium of the Cancer Immunotherapy Consortium
• Thursday, March 17, 2011 7:00 AM - Saturday, March 19, 2011 1:30 PM
Eastern Time
First Speaker: Dr. Rafi Ahmed
Director of the Emory Vaccine Center
"As a basic immunologist, EVC Director Dr. Rafi Ahmed studies immunological memory – the ability of the immune system to “remember” a particular antigen and respond accordingly. Dr. Ahmed and his colleagues have made significant discoveries about how immune memory cells are created and how long they survive; understanding these mechanisms is crucial to the development of vaccines for HIV and other infectious agents. In addition to contributing vitally to vaccine science, Dr. Ahmed’s findings are being applied to research into therapies for the treatment of cancer and the prevention of organ rejection."
Dr. Rafi Ahmed is now being introduced by Johannes Vieweg, & highlighting his work on immunological memory
Dr. Ahmed is sharing how lessons from immune memory development in chronic viral infection can inform cancer immunotherapy field
Ahmed: wait 30-60 days to boost in vaccination produces better immune responses for many types of viral vaccines. Same for cancer?JimmyB :Why 30 to 60 days? Because this is the time factor that it takes for the CD4+ and CD8+ T-cells to grow and differentiate into effector T-cells. (See Graph)
Fig-1
Dr. Rafi Ahmed is now being introduced by Johannes Vieweg, & highlighting his work on immunological memory Dr. Ahmed is sharing how lessons from immune memory development in chronic viral infection can inform cancer immunotherapy field Ahmed: wait 30-60 days to boost in vaccination produces better immune responses for many types of viral vaccines. Same for cancer?
Fig-2
Ahmed: Synergy we've seen combining PD-1 with IL-2 (negative + positive signal) in viral infection therapy have been astonishing.
Jimmy B:Imagine if you combine CTLA-4 + PD-1 and IL-2. The Holy Grail of Immuno therapy I believe.Ahmed raises point that mTOR inhibition may enhance vaccine-induced memory CD8 T-cells. Role for combining with cancer vaccines?
Much audience Q&A for Dr. Ahmed - when see exhaustion clinically, is it inhibition, effect of dose of IL-2, and role of autophagy?
Source: Cancer Research on Twitter
http://twitter.com/#!/search?q=%23cic11
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Labels:
BMS-936558,
CTLA-4,
Dr. Rafi Ahmed,
Emory Vaccine Center,
IL-2,
IL-2 dose timing,
PD-1
Friday, March 4, 2011
Interviews with Laurie and Bob from Melanoma ROADTRIP..Jim Breitfeller
Interviews with Laurie and Bob from Melanoma ROADTRIP
CP:boblawrencesjourney
boblawrencesjourney
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
CP:boblawrencesjourney
boblawrencesjourney
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
Tuesday, March 1, 2011
Breakthrough Drugs Target Deadly Cancer - Boston News Story - WCVB Boston
Combination Therapy BRAF + MEK
When it works, it works quite well.
Breakthrough Drugs Target Deadly Cancer - Boston News Story - WCVB Boston
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
When it works, it works quite well.
Breakthrough Drugs Target Deadly Cancer - Boston News Story - WCVB Boston
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
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Greetings to One and All
This Blog is dedicated My Brother Kenny B. who passed away in the late 1970's with Cancer before the Internet.
It was he, who showed me How to live and give back. He was wise beyond his years.
Jimmy and Dee
Carepage: Jimmybreitfeller
Jimmy Breitfeller
It was he, who showed me How to live and give back. He was wise beyond his years.
Jimmy and Dee
Carepage: Jimmybreitfeller
Jimmy Breitfeller
My Profile as of 2009
- jimmy_B
- Last July (2005)I was riding my bicycle to work at the Eastman Kodak Research Labs about 3 miles from home. I was wearing a knapsack to carry my things to and from the labs. I started noticing an ache on my back. So I decide to go to the dermatologist. To make the long story short, it was cancer. I knew from my research that I would be needing adjuvant therapy. So I started communicating with Sloan Kettering, University of Pittsburgh Cancer Center, and a couple of others including the Wilmot Cancer Center at Strong. I realized that by telling my story, I might help someone else out there in a similar situation. So to all who are linked by diagnosis or by relation to someone with melanoma, I wish you well. Stay positive, read as much as you can (information helps to eliminate the fear associated with the unknown), and live for today, as no one can predict what tomorrow may bring. Jimmy B. posted 12/15/08
Disclaimer
The information contained within this Blog is not meant to replace the examination or advice of your Oncologist or Medical Team. The educational material that is covered here or Linked to, does not cover every detail of each disorder discussed.
Only your physician/Oncologist can make medical decisions and treatment plans that are appropriate for you. But, An Educated Consumer is a Smart consumer.
As Dr. Casey Culberson Said:
"The BEST melanoma patient is an ACTIVE PARTICIPANT in his or her treatment
(not a PASSIVE RECIPIENT)"
Only your physician/Oncologist can make medical decisions and treatment plans that are appropriate for you. But, An Educated Consumer is a Smart consumer.
As Dr. Casey Culberson Said:
"The BEST melanoma patient is an ACTIVE PARTICIPANT in his or her treatment
(not a PASSIVE RECIPIENT)"
Melanoma and the “Magic Bullet” (Monoclonal Antibodies)
Just to let you know I posted the first draft of the Melanoma and the “Magic Bullet” (Monoclonal Antibodies). on Melanoma Missionary In the Shared File Section. you can download it for 19.95 (Only kidding) it is Free for the taking.
It is 33 pages long and may help you in your quest for the Yellow Brick Broad. Just to let you know it is only the first draft. Revisions are sure to come. I wanted to get it to the people that need it the most, the Melanoma Patients.
Preview:
So, where does Interluekin-2 (IL-2) come into play? According to Byung-Scok et al and recent reports, IL-2 is not needed for developmental CD4+ CD25+ Treg cells in the thymus but does play an important role in the maintenance and function in the peripheral.18 Peripheral is defines as secondary system outside the bone marrow and thymus. It entails the site of antigen, immune system interaction. IL-2 is required for the peripheral generation of Tregs based Abbas’s and colleagues research.19
IL-2 prevents the spontaneous apoptosis of the CD4+ CD25+ Treg cells. It has been reported that patients with multiple advance-stage tumors have elevated levels of Tregs within the tumor microenviroment.20 Interluekin-2 is the survival factor for CD4+ CD25+ Treg cells.21 If the addition of IL-2 is on or before the maximum propagation of the CD4+ T cells, the Tregs population can increase 5-fold in a 96 hour period based on certain growth mediums.
By controlling the addition of the endogenous IL-2, one has a knob to turn and can lead to the control of the expansion of the Tregs. When you combined this control with the anti-CTLA-4 blockage, you can shift the balance of the immune response.
Now here is the catch. The maintenance and function of the CD8+ T-cells require CD4+ cells which secrete IL-2. So we don’t want to deplete the CD4+ cells, we want to control the expansion of the Tregs which are a subset of the CD4+ cells. It has been postulated by some researchers that the Anti-CTLA-4 blockage also suppresses the Treg function in a different mechanism. By using IL-2 as the rate limiting factor, we can suppress the CD4+ CD25+ Treg cell expansion by controlling the concentration and timing of the Inerluekin-2 at the tumor microenvironment.
The Interluekin-2 plays another role in this Melanoma Maze. In a study by Janas et al, Il-2 increases the expressions of the perforin and granzyme A, B and C genes in the CD8+ T-cells. This increase expression causes the CD8+ T-cells to mature into Cytoxic T Lymphocytes (CTLs). The exogenous IL-2 is required for the granzyme proteins. As stated previously, CTLs have cytoplasmic granules that contain the proteins perforin and granzymes. A dozen or more perforin molecules insert themselves into the plasma membrane of target cells forming a pore that enables granzymes to enter the cell. Once in the tumor cell, these enzymes are able to breakup (lyse) the cell and destroy it. This is the beginning of the end for the cancer cells. The tumors begin to shrink and the rest is history,
“
On the other hand, prolong therapy with Il-2 can result in causing apoptotic death of the tumor- specific CD8+ T-cells.23
Clearly in a clinical setting, timing, dose, and exposure to these drugs play a major roll in the immunotherapy, and can have dramatic effects on the outcome.
All it takes is that one magic bullet to start the immune reaction..
https://app.box.com/shared/kjgr6dkztj
Melanoma And The Magic Bullet (Monoclonal Antibodies)
It is 33 pages long and may help you in your quest for the Yellow Brick Broad. Just to let you know it is only the first draft. Revisions are sure to come. I wanted to get it to the people that need it the most, the Melanoma Patients.
Preview:
So, where does Interluekin-2 (IL-2) come into play? According to Byung-Scok et al and recent reports, IL-2 is not needed for developmental CD4+ CD25+ Treg cells in the thymus but does play an important role in the maintenance and function in the peripheral.18 Peripheral is defines as secondary system outside the bone marrow and thymus. It entails the site of antigen, immune system interaction. IL-2 is required for the peripheral generation of Tregs based Abbas’s and colleagues research.19
IL-2 prevents the spontaneous apoptosis of the CD4+ CD25+ Treg cells. It has been reported that patients with multiple advance-stage tumors have elevated levels of Tregs within the tumor microenviroment.20 Interluekin-2 is the survival factor for CD4+ CD25+ Treg cells.21 If the addition of IL-2 is on or before the maximum propagation of the CD4+ T cells, the Tregs population can increase 5-fold in a 96 hour period based on certain growth mediums.
By controlling the addition of the endogenous IL-2, one has a knob to turn and can lead to the control of the expansion of the Tregs. When you combined this control with the anti-CTLA-4 blockage, you can shift the balance of the immune response.
Now here is the catch. The maintenance and function of the CD8+ T-cells require CD4+ cells which secrete IL-2. So we don’t want to deplete the CD4+ cells, we want to control the expansion of the Tregs which are a subset of the CD4+ cells. It has been postulated by some researchers that the Anti-CTLA-4 blockage also suppresses the Treg function in a different mechanism. By using IL-2 as the rate limiting factor, we can suppress the CD4+ CD25+ Treg cell expansion by controlling the concentration and timing of the Inerluekin-2 at the tumor microenvironment.
The Interluekin-2 plays another role in this Melanoma Maze. In a study by Janas et al, Il-2 increases the expressions of the perforin and granzyme A, B and C genes in the CD8+ T-cells. This increase expression causes the CD8+ T-cells to mature into Cytoxic T Lymphocytes (CTLs). The exogenous IL-2 is required for the granzyme proteins. As stated previously, CTLs have cytoplasmic granules that contain the proteins perforin and granzymes. A dozen or more perforin molecules insert themselves into the plasma membrane of target cells forming a pore that enables granzymes to enter the cell. Once in the tumor cell, these enzymes are able to breakup (lyse) the cell and destroy it. This is the beginning of the end for the cancer cells. The tumors begin to shrink and the rest is history,
“
On the other hand, prolong therapy with Il-2 can result in causing apoptotic death of the tumor- specific CD8+ T-cells.23
Clearly in a clinical setting, timing, dose, and exposure to these drugs play a major roll in the immunotherapy, and can have dramatic effects on the outcome.
All it takes is that one magic bullet to start the immune reaction..
https://app.box.com/shared/kjgr6dkztj
Melanoma And The Magic Bullet (Monoclonal Antibodies)
Public Service Announcement
A call for Melanoma Patients by Dr. Steven A Rosenberg
"We continue to see a high rate of clinical responses in our cell transfer immunotherapy treatments for patients with metastatic melanoma", Dr. Rosenberg said.
"We are actively seeking patients for these trials and any note of that on a patient-directed web site would be appreciated."
If you would like to apply for his trials, here is the website and information.
Dr. Rosenberg's information
Dr. Rosenberg's Clinical Trials
The Melanoma Research Alliance has partnered with Bruce Springsteen, the E Street Band, and the Federici family to alleviate suffering and death from melanoma. Please view Bruce Springsteen’s public service announcement inspired by Danny Federici. Danny was the E Street Band’s organist and keyboard player. He died on April 17, 2008 at Memorial Sloan-Kettering Cancer Center in New York City after a three year battle with melanoma.
http://www.melanomaresearchalliance.org/news/PSA/
Source Fastcures blog
"We continue to see a high rate of clinical responses in our cell transfer immunotherapy treatments for patients with metastatic melanoma", Dr. Rosenberg said.
"We are actively seeking patients for these trials and any note of that on a patient-directed web site would be appreciated."
If you would like to apply for his trials, here is the website and information.
Dr. Rosenberg's information
Dr. Rosenberg's Clinical Trials
The Melanoma Research Alliance has partnered with Bruce Springsteen, the E Street Band, and the Federici family to alleviate suffering and death from melanoma. Please view Bruce Springsteen’s public service announcement inspired by Danny Federici. Danny was the E Street Band’s organist and keyboard player. He died on April 17, 2008 at Memorial Sloan-Kettering Cancer Center in New York City after a three year battle with melanoma.
http://www.melanomaresearchalliance.org/news/PSA/
Source Fastcures blog
Join the Relay for Life!!!
Dear Family and Friends,
I’ve decided to take a stand and fight back against cancer by participating in the American Cancer Society Relay For Life® event right here in my community! Please support me in this important cause by making a secure, tax-deductible donation online using the link below.
To donate on line now, click here to visit my personal page.
Jimmy B AKA Melanoma_Missionary
Relay For Life® is a life-changing event that brings together more than 3.5 million people worldwide to:
CELEBRATE the lives of those who have battled cancer. The strength of survivors inspires others to continue to fight.
REMEMBER loved ones lost to the disease. At Relay, people who have walked alongside people battling cancer can grieve and find healing.
FIGHT BACK. We Relay because we have been touched by cancer and desperately want to put an end to the disease.
Whatever you can give will help - it all adds up! I greatly appreciate your support and will keep you posted on my progress.
Keep the Fire Burning!!!
Sincerely,
Jimmy Breitfeller
Turn off Music before you "Click to Play"
Signs of Melanoma Carcinoma Skin Cancer
Signs of Melanoma Carcinoma Skin Cancer
How Skin Cancer Develops by "About.com : Dermatology"
Call for Patients with Unresectable Liver Metastases Due to Melanoma
Delcath Systems Granted Orphan-Drug Designations for Cutaneous and Ocular Melanoma
Delcath is actively enrolling patients in a Phase III clinical trial testing its proprietary drug delivery system, known as Percutaneous Hepatic Perfusion (“PHP”), with melphalan for the treatment of ocular and cutaneous melanoma metastatic to the liver.
This NCI-led trial is enrolling patients at leading cancer centers throughout the United States. Commenting on these orphan-drug designations, Richard L. Taney, President and CEO of Delcath, stated, “These favorable designations are important steps in our efforts to secure Delcath’s commercial position upon conclusion of our pivotal Phase III trial for metastatic melanoma. We remain steadfast in our commitment to become the leader in the regional treatment of liver cancers and we continue to enroll patients in this study, and advance our technology and the promise that it offers to patients with these deadly forms of melanoma and other cancers of the liver, all with limited treatment options.”
Orphan drug designation, when granted by the FDA’s Office of Orphan Products Development, allows for up to seven years of market exclusivity upon FDA approval, as well as clinical study incentives, study design assistance, waivers of certain FDA user fees, and potential tax credits.
Current Trial Centers
Phase I Study of Hepatic Arterial Melphalan Infusion and Hepatic Venous Hemofiltration Using
Percutaneously Placed Catheters in Patients With Unresectable Hepatic Malignancies
James F. Pingpank, Jr., MD, FACS
Associate Professor of Surgery
Division of Surgical Oncology
Suite 406, UPMC Cancer Pavillion
5150 Centre Avenue
Pittsburgh, PA 15232
412-692-2852 (Office)
412-692-2520 (Fax)
PingpankJF@UPMC.edu
Delcath Systems Granted Orphan-Drug Designations for Cutaneous and Ocular Melanoma
Delcath is actively enrolling patients in a Phase III clinical trial testing its proprietary drug delivery system, known as Percutaneous Hepatic Perfusion (“PHP”), with melphalan for the treatment of ocular and cutaneous melanoma metastatic to the liver.
This NCI-led trial is enrolling patients at leading cancer centers throughout the United States. Commenting on these orphan-drug designations, Richard L. Taney, President and CEO of Delcath, stated, “These favorable designations are important steps in our efforts to secure Delcath’s commercial position upon conclusion of our pivotal Phase III trial for metastatic melanoma. We remain steadfast in our commitment to become the leader in the regional treatment of liver cancers and we continue to enroll patients in this study, and advance our technology and the promise that it offers to patients with these deadly forms of melanoma and other cancers of the liver, all with limited treatment options.”
Orphan drug designation, when granted by the FDA’s Office of Orphan Products Development, allows for up to seven years of market exclusivity upon FDA approval, as well as clinical study incentives, study design assistance, waivers of certain FDA user fees, and potential tax credits.
Current Trial Centers
Phase I Study of Hepatic Arterial Melphalan Infusion and Hepatic Venous Hemofiltration Using
Percutaneously Placed Catheters in Patients With Unresectable Hepatic Malignancies
James F. Pingpank, Jr., MD, FACS
Associate Professor of Surgery
Division of Surgical Oncology
Suite 406, UPMC Cancer Pavillion
5150 Centre Avenue
Pittsburgh, PA 15232
412-692-2852 (Office)
412-692-2520 (Fax)
PingpankJF@UPMC.edu
Blog Archive
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2011
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March
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- A call for patients that failed PLX-4032 Melanoma ...
- Profitable are the sick, for they shall be exploit...
- F.D.A. Approves Drug to Treat Melanoma..Jim Breitf...
- Late-Breaking Abstracts..Melanoma ..Jim Breitfeller
- Bristol-Myers Awaits Approval for Drug's New Cance...
- Sounding the Danger Signal through chemotherapy to...
- “Schedule and Dose for Combination Therapy,” Melan...
- Interviews with Laurie and Bob from Melanoma ROADT...
- Breakthrough Drugs Target Deadly Cancer - Boston N...
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March
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Call For Melanoma Patients!!!!
Call For Melanoma Patients!!!!
Dr. Rosenberg Has a New Clinical Trial.
Our latest treatment has a 72% objective response rate with 36% complete responses.
We are currently recruiting patients for our latest trial.
Is there some way to post this “Call for Patients” on the web site?
Steve Rosenberg
Dr. Rosenberg's Clinical Trials
(For a copy of the research paper.. see My Shared files)
Dr. Rosenberg Has a New Clinical Trial.
Our latest treatment has a 72% objective response rate with 36% complete responses.
We are currently recruiting patients for our latest trial.
Is there some way to post this “Call for Patients” on the web site?
Steve Rosenberg
Dr. Rosenberg's Clinical Trials
(For a copy of the research paper.. see My Shared files)
The news headlines shown above for Melanoma / Skin Cancer are provided courtesy of Medical News Today.