Results from Three Phase 2 Studies Reported a Two-Year Survival Rate Ranging from 30 to 42 Percent in Metastatic Melanoma Patients Treated with Ipilimumab (10 mg/kg)
PRINCETON, N.J.--(BUSINESS WIRE)--May. 31, 2009--Bristol-Myers
Squibb Company (NYSE: BMY) and Medarex,
Inc. (NASDAQ: MEDX) today announced updated survival results from
follow-up extensions of three Phase 2 ipilimumab studies of patients
with advanced metastatic melanoma (Stage III or IV). The two-year
survival rate ranged from 29.8 to 41.8 percent in patients who received
ipilimumab (10 mg/kg). Results of the survival data were presented at
the 45th Annual Meeting of the American Society of Clinical
Oncology in Orlando, FL., May 29 -- June 2, 2009.
The results are based on follow-up of up to 37.5 months (median
follow-up ranging from 10.1 to 16.3 months) of the patient population
from studies 008, 022 and 007 treated with 10 mg/kg of ipilimumab
(induction and maintenance) and, specifically, showed:
Two-year survival rate of 32.8 percent (95% CI: 25.37%- 40.49%) in
patients who had progressed while on or after receiving standard
treatment (Study 008, Abstract #9033);
Two-year survival rate of 29.8 percent (95% CI: 19.13%- 41.14%) in
patients who were previously treated, relapsed or failed to respond to
experimental treatment or were unable to tolerate currently approved
therapies (Study 022, Abstract #9033);
Two-year survival rate of 40.6 percent (95% CI: 27.12%- 54.37%) and
41.8 percent (95% CI: 28.30%- 55.46%) in patients receiving ipilimumab
plus budesonide or ipilimumab plus placebo, respectively, which
included treatment-naïve patients and patients previously treated with
therapy other than ipilimumab (Study 007, Abstract #9033).
Historical melanoma survival rates from previous clinical trials have
been estimated by a recent meta-analysis of 42 Phase 2 trials of over
2,100 patients with Stage III or IV metastatic melanoma indicating that,
at one year, approximately 25 percent of patients were alive. Results
from three separately published randomized Phase 3 studies using
dacarbazine as the control arm reported that, at two years,
approximately 8 to 12 percent of metastatic melanoma patients were alive.
The updated survival analyses did not include additional safety data. As
previously reported, safety results include follow-up of up to 16.3
months with a median follow-up ranging from 4.7 to 5.65 months. The most
common immune-related adverse events were rash, diarrhea and hepatitis.
Grade 3 and 4 immune-related adverse event rates were approximately 20
to 29 percent and zero to 12 percent, respectively, in patients who
received 10 mg/kg of ipilimumab. Adverse events were managed with the
use of supportive care and systemic steroids using established treatment
guidelines in the majority of patients. Additionally, the use of
systemic steroids to manage adverse events does not appear to diminish
or impact the clinical effect of ipilimumab (Abstract #9037).
"The ongoing survival data observed with ipilimumab are encouraging,
particularly because the advanced melanoma patient population currently
has limited treatment options," said Steven J. O'Day, M.D., Chief of
Research and Director of the Melanoma Program at The Angeles Clinic and
Research Institute, California. "The potential of ipilimumab is also
underscored by the fact that we can report two-year survival results
from these studies involving a significant number of metastatic melanoma
patients."
Candidate Biomarkers of Ipilimumab
Researchers also presented an exploratory analysis from four Phase 2
ipilimumab studies (008, 022, 007 and 004) that looked at the
association between clinical activity and multiple potential biomarkers,
including the change in absolute lymphocyte count (ALC) in melanoma
patients after they received ipilimumab (Abstracts #9008 and #3020). ALC
is a measure of the number of immune cells in circulation.
In a combined analysis of studies 007, 008 and 022, clinical activity
was associated with an increase in the rate of change in ALC. Patients
with clinical activity had a higher average increase in ALC over time
than did patients without clinical activity (P=0.0013) and no patient
with a decrease in ALC over time had clinical activity. This association
was separately confirmed in Study 004. Increases in ALC following
administration of ipilimumab were also significantly associated with
dose (studies 007, 008, 022: P<0.0001; study 004: P=0.0015), favoring
the 10 mg/kg regimen. Based on these early biomarker findings, further
research to explore the implication of ALC and other potential
biomarkers of clinical activity of ipilimumab continues.
About Studies 008, 022 and 007
The three studies enrolled a total of 487
patients across North
America, Europe, South America, Africa and Australia with Stage III or
Stage IV metastatic melanoma treated with ipilimumab therapy (0.3 mg/kg,
3.0 mg/kg or 10 mg/kg every three weeks for up to four doses, followed
by maintenance dosing every 12 weeks). Specifically, the three Phase 2
monotherapy trials include:
A Phase 2 open-label, single-arm trial (008) evaluating overall
response rate in 155 patients who progressed while on or after
receiving standard treatment;
A Phase 2 randomized, double-blind trial (022) evaluating the efficacy
of three dose levels of ipilimumab in 217 patients who were previously
treated, relapsed or failed to respond to experimental treatment or
were unable to tolerate currently approved therapies; and
A Phase 2 randomized, double-blind trial (007) evaluating the rate of
Grade 2+ diarrhea in 115 patients receiving ipilimumab with or without
prophylactic oral budesonide.
The primary endpoint of studies 008 and 022 was best overall response
rate and the primary endpoint of study 007 was to compare the rate of
Grade 2+ diarrhea in patients receiving ipilimumab with or without
prophylactic oral budesonide. Overall survival, one-year survival rates,
disease control rate, stable disease, and other measurements of
anti-tumor activity and patterns of responses were secondary endpoints
in studies 008, 022 and 007. The two-year survival data reported are
current (through March, 2009) for all subjects followed: 93.6% from
study 008, 91.7% from study 022 and 84.2% and 82.8% from the two
subgroups of study 007 (placebo and budesonide, respectively).
About Study 004
Study 004 is a Phase 2 randomized, double-blind biomarker trial. The
study enrolled 82 patients with advanced melanoma who were previously
treated with therapy other than ipilimumab or who received no prior
therapy. All patients received ipilimumab therapy (3.0 mg/kg or 10
mg/kg). Pre- and post-treatment (week four) tumor biopsies were
performed to assess associations between tumor biomarkers and clinical
activity of ipilimumab. Clinical activity was defined as complete or
partial response or stable disease at ≥24 weeks using modified World
Health Organization criteria.
Sunday, May 31, 2009
Experts Optimistic About Melanoma vaccine.. Melanoma..Jim Breitfeller
tPhase 3 study reports improved survival for those with advanced disease,,
SATURDAY, May 30 (HealthDay News) --A vaccine for advanced melanoma has shown promise in a new study.
Melanoma is the most serious type of skin cancer. The five year-survival rates for local and metastatic melanoma are 65 percent and 16 percent, respectively. In 2009, an estimated 69,000 people in the United States will be diagnosed with melanoma and about 8,600 will die of the disease, according to the American Cancer Society.
The study, a phase 3 clinical trial involving 185 people, found that using the peptide vaccine in combination with the immunotherapy drug Interleukin-2 improved response rates and progression-free survival, according to University of Texas M.D. Anderson Cancer Center researchers, who said it was the first phase 3 trial to show a clinical benefit in a vaccine for melanoma.
Response rate and progression-free survival were 22.1 percent and 2.9 months, respectively, in people given the vaccine, compared with 9.7 percent and 1.6 months for those who were not vaccinated. Median overall survival was 17.6 months for the vaccine group and 12.8 months for the others.
The study, which was to be presented Saturday at the annual meeting of the American Society of Clinical Oncology in Orlando, Fla., was funded in part by Novartis, which makes Interleukin-2.
"Obviously this is a disease, in its advanced setting, in need of better therapies for our patients," study co-author Dr. Patrick Hwu, a professor and chairman of M.D. Anderson's Department of Melanoma Medical Oncology, said in a news release from the center.
"While more follow-up is needed, this study serves as a proof-of-principle for vaccines' role in melanoma and in cancer therapy overall," Hwu said. "If we can use the body's own defense system to attack tumor cells, we provide a mechanism for ridding the body of cancer without destroying healthy tissue."
The vaccine, called gp100:209-217 (200M), works by stimulating T-cells, which control immune response.
"This vaccine activates the body's cytotoxic T-cells to recognize antigens on the surface of the tumor," Hwu said. "The T-cells then secrete enzymes that poke holes in the tumor cell's membrane, causing it to disintegrate."
Source:http://www.bio-medicine.org/medicine-news-1/Experts-Optimistic-About-Melanoma-Vaccine--47378-1/
SATURDAY, May 30 (HealthDay News) --A vaccine for advanced melanoma has shown promise in a new study.
Melanoma is the most serious type of skin cancer. The five year-survival rates for local and metastatic melanoma are 65 percent and 16 percent, respectively. In 2009, an estimated 69,000 people in the United States will be diagnosed with melanoma and about 8,600 will die of the disease, according to the American Cancer Society.
The study, a phase 3 clinical trial involving 185 people, found that using the peptide vaccine in combination with the immunotherapy drug Interleukin-2 improved response rates and progression-free survival, according to University of Texas M.D. Anderson Cancer Center researchers, who said it was the first phase 3 trial to show a clinical benefit in a vaccine for melanoma.
Response rate and progression-free survival were 22.1 percent and 2.9 months, respectively, in people given the vaccine, compared with 9.7 percent and 1.6 months for those who were not vaccinated. Median overall survival was 17.6 months for the vaccine group and 12.8 months for the others.
The study, which was to be presented Saturday at the annual meeting of the American Society of Clinical Oncology in Orlando, Fla., was funded in part by Novartis, which makes Interleukin-2.
"Obviously this is a disease, in its advanced setting, in need of better therapies for our patients," study co-author Dr. Patrick Hwu, a professor and chairman of M.D. Anderson's Department of Melanoma Medical Oncology, said in a news release from the center.
"While more follow-up is needed, this study serves as a proof-of-principle for vaccines' role in melanoma and in cancer therapy overall," Hwu said. "If we can use the body's own defense system to attack tumor cells, we provide a mechanism for ridding the body of cancer without destroying healthy tissue."
The vaccine, called gp100:209-217 (200M), works by stimulating T-cells, which control immune response.
"This vaccine activates the body's cytotoxic T-cells to recognize antigens on the surface of the tumor," Hwu said. "The T-cells then secrete enzymes that poke holes in the tumor cell's membrane, causing it to disintegrate."
Source:http://www.bio-medicine.org/medicine-news-1/Experts-Optimistic-About-Melanoma-Vaccine--47378-1/
Friday, May 29, 2009
Despite Past Disappointments the Future of Melanoma Therapy Appears Bright Melanoma..Jim Breitfeller
Ahmad Tarhini, MD, MSc
Assistant Professor of Medicine
Department of Medicine
Division of Hematology/Oncology
University of Pittsburgh School of Medicine
Annually, about 8,000 patients are found to have metastatic melanoma presenting as recurrence of an earlier primary melanoma, and this number closely approximates the annual number of deaths from the disease. This statistic illustrates the lack of progress that has been made in the treatment of stage IV melanoma over the past several decades. As very nicely reviewed in this issue of ONCOLOGY by Bhatia et al, no therapeutic agent has been shown in randomized clinical trials to prolong survival in patients with metastatic melanoma. Chemotherapy with single-agent dacarbazine is the only US Food and Drug Administration (FDA)-approved chemotherapy agent for metastatic melanoma.
Role of Immunity
Immunity to melanoma appears to be important for disease control in the adjuvant and advanced-disease settings. Spontaneous regression has been reported in melanoma, suggesting a role for host immunity. This possibility is indirectly supported by the regular presence of lymphoid infiltrates at the site of primary melanoma, a phenomenon that is frequently associated with histopathologic evidence of tumor regression.
Host cellular immune response within melanoma has potential prognostic and predictive significance. T-cell infiltrates in primary melanoma are prognostic of disease outcome,[1] and T-cell infiltrates within regional nodal metastasis predict benefit from interferon alfa-2b (IFNα2b, Intron A) therapy.[2-4] Immunologic approaches have yielded the only newly FDA-approved agent for metastatic disease in 30 years—high-dose bolus interleukin-2 (IL-2, Proleukin). This therapy is based on durable responses seen in some patients with metastatic melanoma, but with an associated high toxicity rate and cost.
Novel Agents
Currently the optimal approach to the management of patients with metastatic melanoma is treatment on clinical trials in an effort to maximize treatment options and provide access to promising therapeutic approaches for this disease. The future of melanoma therapy appears promising, with many novel experimental agents being tested in clinic, building upon the continuously deepening knowledge of host immunity and molecular circuitry of the tumor. Cancer vaccines continue to be actively tested in melanoma (peptide vaccines, genetic heat shock proteins, and dendritic cell–based vaccines). Molecular approaches to deranged signaling pathways and proapoptotic strategies are also being widely investigated. A phase III intergroup trial coordinated by the Eastern Cooperative Oncology Group (E2603) was recently completed, in which 800 patients with chemotherapy-naive metastatic melanoma were randomized to carboplatin and paclitaxel with either sorafenib (Nexavar) or placebo. The results of this trial are awaited. The roles of several critical regulatory elements of the immune system have recently been elucidated, providing insight into the disease process and new targets for overcoming tolerance. Enhanced expression of costimulatory molecules on the surface of dendritic cells is one approach to enhancing the presentation of tumor-associated antigens. This can be achieved through stimulation of dendritic cell receptors such as CD40 and Toll-like receptor 9 (TLR9).[57] Another approach is to enhance or prolong T-cell activation by blocking negative-signaling receptors such as CTLA4.[8] New strategies, such as the administration of oligodeoxynucleotides that activate TLR9, monoclonal antibodies (mAbs) that activate CD40 or block CTLA4, and costimulatory antibodies to CD137, or targeting regulators of apoptosis such as PD1 (programmed death-1)[9] may provide more effective immunotherapies that might overcome tumor-induced tolerance.
The closure of the tremelimumab phase III melanoma study for “futility” came as a surprise to many investigators, given clinical observations of durable benefits in some patients. The 1-year survival rate of > 50% for tremelimumab and the median survival of 11.7 months (compared with 10.7 months for chemotherapy) were also surprising, although this may have been the result of the selection criteria for this study. The exclusion of patients with 2× upper limit of normal lactate dehydrogenase (LDH) blood values and crossover of patients in the control arm to another anti-CTLA4 mAb may also have played a role in the results, but this remains to be clarified, and more mature survival and response data are anticipated. Results of the phase III studies testing CTLA4 blockade with ipilimumab (as a single agent or in combination with dacarbazine in one study, and administered in conjunction with the gp100 peptide vaccine in another study) are eagerly anticipated.
The further development of novel agents in melanoma will likely include combinations based on strategies for overcoming tumor-induced immune suppression. Preliminary data from combination biotherapy involving CTLA4-blockade with high-dose IFN-α2b[10] and dendritic cell–based vaccination are promising in melanoma.[9,11,12]
Biomarkers
Future research should incorporate the study of biomarkers to predict therapeutic benefit into randomized trials. This may lead to the identification of biomarkers enabling personalized therapy, which has become a Holy Grail of sorts, particularly in melanoma, for which standard options are so limited. Although subsets of melanoma patients clearly benefit from different approaches, these positive results have not been reproduced in classic randomized trials. Some clues could be found in the now repeatedly reported association between the induction of autoimmunity and therapeutic benefit with IFN-α2b, IL-2, and CTLA4-blocking mAbs.[13] Revealing investigations might involve the induction of autoimmunity to a broad array of endocrine and tumor markers as biomarkers of therapeutic benefit.
In addition, researchers may identify immunogenetic factors that predispose patients to induction of autoimmunity by these agents (eg, human leukocyte antigen genotype, polymorphisms of the CTLA4 gene and the FOXP3 transcription factor loci, as well as other immunogenetic markers). Multiplex analysis—encompassing cytokines, chemokines, angiogenic and growth factors, soluble receptors, signal transduction molecules, and other immune and endocrine markers—in relation to patient outcome could also be studied, building upon promising early results.[13,14] Important data along these lines could be provided from melanoma patients treated with adjuvant high-dose IFN-α2b (E1697), and planned adjuvant trials with CTLA4 blockade (ipilimumab, E1609).
source:http://www.cancernetwork.com/cme/article/10165/1415169
Take care
Assistant Professor of Medicine
Department of Medicine
Division of Hematology/Oncology
University of Pittsburgh School of Medicine
Annually, about 8,000 patients are found to have metastatic melanoma presenting as recurrence of an earlier primary melanoma, and this number closely approximates the annual number of deaths from the disease. This statistic illustrates the lack of progress that has been made in the treatment of stage IV melanoma over the past several decades. As very nicely reviewed in this issue of ONCOLOGY by Bhatia et al, no therapeutic agent has been shown in randomized clinical trials to prolong survival in patients with metastatic melanoma. Chemotherapy with single-agent dacarbazine is the only US Food and Drug Administration (FDA)-approved chemotherapy agent for metastatic melanoma.
Role of Immunity
Immunity to melanoma appears to be important for disease control in the adjuvant and advanced-disease settings. Spontaneous regression has been reported in melanoma, suggesting a role for host immunity. This possibility is indirectly supported by the regular presence of lymphoid infiltrates at the site of primary melanoma, a phenomenon that is frequently associated with histopathologic evidence of tumor regression.
Host cellular immune response within melanoma has potential prognostic and predictive significance. T-cell infiltrates in primary melanoma are prognostic of disease outcome,[1] and T-cell infiltrates within regional nodal metastasis predict benefit from interferon alfa-2b (IFNα2b, Intron A) therapy.[2-4] Immunologic approaches have yielded the only newly FDA-approved agent for metastatic disease in 30 years—high-dose bolus interleukin-2 (IL-2, Proleukin). This therapy is based on durable responses seen in some patients with metastatic melanoma, but with an associated high toxicity rate and cost.
Novel Agents
Currently the optimal approach to the management of patients with metastatic melanoma is treatment on clinical trials in an effort to maximize treatment options and provide access to promising therapeutic approaches for this disease. The future of melanoma therapy appears promising, with many novel experimental agents being tested in clinic, building upon the continuously deepening knowledge of host immunity and molecular circuitry of the tumor. Cancer vaccines continue to be actively tested in melanoma (peptide vaccines, genetic heat shock proteins, and dendritic cell–based vaccines). Molecular approaches to deranged signaling pathways and proapoptotic strategies are also being widely investigated. A phase III intergroup trial coordinated by the Eastern Cooperative Oncology Group (E2603) was recently completed, in which 800 patients with chemotherapy-naive metastatic melanoma were randomized to carboplatin and paclitaxel with either sorafenib (Nexavar) or placebo. The results of this trial are awaited. The roles of several critical regulatory elements of the immune system have recently been elucidated, providing insight into the disease process and new targets for overcoming tolerance. Enhanced expression of costimulatory molecules on the surface of dendritic cells is one approach to enhancing the presentation of tumor-associated antigens. This can be achieved through stimulation of dendritic cell receptors such as CD40 and Toll-like receptor 9 (TLR9).[57] Another approach is to enhance or prolong T-cell activation by blocking negative-signaling receptors such as CTLA4.[8] New strategies, such as the administration of oligodeoxynucleotides that activate TLR9, monoclonal antibodies (mAbs) that activate CD40 or block CTLA4, and costimulatory antibodies to CD137, or targeting regulators of apoptosis such as PD1 (programmed death-1)[9] may provide more effective immunotherapies that might overcome tumor-induced tolerance.
The closure of the tremelimumab phase III melanoma study for “futility” came as a surprise to many investigators, given clinical observations of durable benefits in some patients. The 1-year survival rate of > 50% for tremelimumab and the median survival of 11.7 months (compared with 10.7 months for chemotherapy) were also surprising, although this may have been the result of the selection criteria for this study. The exclusion of patients with 2× upper limit of normal lactate dehydrogenase (LDH) blood values and crossover of patients in the control arm to another anti-CTLA4 mAb may also have played a role in the results, but this remains to be clarified, and more mature survival and response data are anticipated. Results of the phase III studies testing CTLA4 blockade with ipilimumab (as a single agent or in combination with dacarbazine in one study, and administered in conjunction with the gp100 peptide vaccine in another study) are eagerly anticipated.
The further development of novel agents in melanoma will likely include combinations based on strategies for overcoming tumor-induced immune suppression. Preliminary data from combination biotherapy involving CTLA4-blockade with high-dose IFN-α2b[10] and dendritic cell–based vaccination are promising in melanoma.[9,11,12]
Biomarkers
Future research should incorporate the study of biomarkers to predict therapeutic benefit into randomized trials. This may lead to the identification of biomarkers enabling personalized therapy, which has become a Holy Grail of sorts, particularly in melanoma, for which standard options are so limited. Although subsets of melanoma patients clearly benefit from different approaches, these positive results have not been reproduced in classic randomized trials. Some clues could be found in the now repeatedly reported association between the induction of autoimmunity and therapeutic benefit with IFN-α2b, IL-2, and CTLA4-blocking mAbs.[13] Revealing investigations might involve the induction of autoimmunity to a broad array of endocrine and tumor markers as biomarkers of therapeutic benefit.
In addition, researchers may identify immunogenetic factors that predispose patients to induction of autoimmunity by these agents (eg, human leukocyte antigen genotype, polymorphisms of the CTLA4 gene and the FOXP3 transcription factor loci, as well as other immunogenetic markers). Multiplex analysis—encompassing cytokines, chemokines, angiogenic and growth factors, soluble receptors, signal transduction molecules, and other immune and endocrine markers—in relation to patient outcome could also be studied, building upon promising early results.[13,14] Important data along these lines could be provided from melanoma patients treated with adjuvant high-dose IFN-α2b (E1697), and planned adjuvant trials with CTLA4 blockade (ipilimumab, E1609).
source:http://www.cancernetwork.com/cme/article/10165/1415169
Take care
Thursday, May 28, 2009
Friday, May 22, 2009
Data Mining... Melanoma...Jim Breitfeller
Source:http://www.curehunter.com/public/keywordSummaryD008545.do
Cure Hunter Melanoma
Take care
Jimmy B
Thursday, May 21, 2009
CTLA4 blockade increases Th17 cells in patients with metastatic melanoma. Jim Breitfeller
"From this work we conclude that Th17 cells may be implicated in the clinical effects of CTLA4 blocking monoclonal antibodies, and further study of their role in treatment-induced toxicities may help in elucidating how toxicities and responses may be differentially modulated with this mode of therapy."
Source:CTLA4 blockade increases Th17 cells in patients with metastatic melanoma.
Since I had a inflamatory response, I need to futher investagate the Th17 cells.
Jimmy B
Source:CTLA4 blockade increases Th17 cells in patients with metastatic melanoma.
Since I had a inflamatory response, I need to futher investagate the Th17 cells.
Jimmy B
Friday, May 15, 2009
Proof-of-concept for V600E BRAF mutation as a therapeutic target in human cancer..Melanoma..Jim Breitfeller
Proof-of-concept for V600E BRAF mutation as a therapeutic target in human cancer
Phase 1 study of PLX4032: Proof-of-concept for V600E BRAF mutation as a therapeutic target in human cancer”
Oral presentation to be made on June 1, 2009, 4:30 p.m. to 6:00 p.m. EDT by Keith T. Flaherty, assistant professor, University of Pennsylvania Abramson Cancer Center, in the “Molecular Phenotype of Melanoma Subtypes and Patient-Specific Therapy” session
Link to video clip of Dr. Flaherty
We just may be getting a handle on this deadly disease!!!!!!!!!
Take care
Jimmy B
Phase 1 study of PLX4032: Proof-of-concept for V600E BRAF mutation as a therapeutic target in human cancer”
Oral presentation to be made on June 1, 2009, 4:30 p.m. to 6:00 p.m. EDT by Keith T. Flaherty, assistant professor, University of Pennsylvania Abramson Cancer Center, in the “Molecular Phenotype of Melanoma Subtypes and Patient-Specific Therapy” session
Link to video clip of Dr. Flaherty
We just may be getting a handle on this deadly disease!!!!!!!!!
Take care
Jimmy B
Thursday, May 14, 2009
Ipilimumab linked to melanoma survival: studies..Melanoma..Jim Breitfeller
Thu May 14, 2009 6:01pm EDT
LOS ANGELES, May 14 (Reuters) - More than a third of advanced melanoma patients treated with ipilimumab, an antibody being developed by Bristol-Myers Squibb Co (BMY.N) and Medarex Inc (MEDX.O), continued to survive after 18 months, according to data released on Thursday.
The 18-month survival rate for three Phase 2 trials ranged from 34.5 percent to 39.4 percent. Most trial participants had been previously treated with other therapies.
"The median survival in the past was only six months," said Renzo Canetta, head of oncology research at Bristol-Myers.
Two-year survival results are slated for presentation later this month at a meeting of the American Society of Clinical Oncology in Orlando.
Bristol-Myers and Medarex said last year that they would delay seeking approval of the experimental treatment after U.S. health regulators asked for additional overall survival data to further demonstrate the benefit of ipilimumab.
Canetta said Phase 3 data for ipilimumab in melanoma patients is expected to mature toward the end of this year or early 2010.
Ipilimumab is a fully human antibody that binds to a molecule on T-cells that plays a critical role in regulating natural immune responses to disease. The drug is also being studied in other tumor types, including lung cancer and prostate cancer.
Source:http://www.reuters.com/article/marketsNews/idUSN1434063520090514
Take care
Jimmy B
LOS ANGELES, May 14 (Reuters) - More than a third of advanced melanoma patients treated with ipilimumab, an antibody being developed by Bristol-Myers Squibb Co (BMY.N) and Medarex Inc (MEDX.O), continued to survive after 18 months, according to data released on Thursday.
The 18-month survival rate for three Phase 2 trials ranged from 34.5 percent to 39.4 percent. Most trial participants had been previously treated with other therapies.
"The median survival in the past was only six months," said Renzo Canetta, head of oncology research at Bristol-Myers.
Two-year survival results are slated for presentation later this month at a meeting of the American Society of Clinical Oncology in Orlando.
Bristol-Myers and Medarex said last year that they would delay seeking approval of the experimental treatment after U.S. health regulators asked for additional overall survival data to further demonstrate the benefit of ipilimumab.
Canetta said Phase 3 data for ipilimumab in melanoma patients is expected to mature toward the end of this year or early 2010.
Ipilimumab is a fully human antibody that binds to a molecule on T-cells that plays a critical role in regulating natural immune responses to disease. The drug is also being studied in other tumor types, including lung cancer and prostate cancer.
Source:http://www.reuters.com/article/marketsNews/idUSN1434063520090514
Take care
Jimmy B
Wednesday, May 13, 2009
The Role of the CTLA-4/PD-1 Pathway in Regulating T-Cell Response..Melanoma ..Jim Breitfeller
The Role of the CTLA-4/PD-1 Pathway in Regulating T-Cell Response
Jeffrey Weber, MD, PhD
The Role of the CTLA-4/PD-1 Pathway in Regulating T-Cell Response Flash Presentation
For those looking of information
Jimmy B
Jeffrey Weber, MD, PhD
The Role of the CTLA-4/PD-1 Pathway in Regulating T-Cell Response Flash Presentation
For those looking of information
Jimmy B
IL-2 vs Anti-CTLA-4 Survival Data!! Melanoma..Jim Breitfeller
The Immune System as a Target for Therapy: Improving Immune Responses and Breaking Tolerance
Moderators
Antoni Ribas, MD
Dirk Schadendorf, MD
First Global Workshop on Malignant Melanoma Nov 30-Dec 1, 2007, Fajardo, Puerto Rico
Ribas
Take care
Jimmy B
Moderators
Antoni Ribas, MD
Dirk Schadendorf, MD
First Global Workshop on Malignant Melanoma Nov 30-Dec 1, 2007, Fajardo, Puerto Rico
Ribas
Take care
Jimmy B
Friday, May 8, 2009
Treatment options for metastatic melanoma. A systematic review..Melanoma ..Jim Breitfeller
Received: 12 January 2009; Revised: 9 March 2009
Accepted: 13 March 2009; electronically published: April 2009
Summary
"Metastatic melanoma is considered to be one of the most resistant tumors to standard chemotherapy approaches nowadays. Old anti-cancer treatments like dacarbacin (DTIC) or interleukin-2 (IL-2) continue to be the only approved treatments by the main worldwide health authorities. Up to now, no combination or new anti-targeted agent has shown an improvement in overall survival when compared to either of these two drugs alone. In fact, more than a dozen phase III randomized trials have tried to go beyond these old approaches, without meeting any success. Despite the fact that the median overall survival of patients diagnosed with metastatic melanoma is lower than 9 months, melanoma emerges as a challenging disease for testing new drugs and implementing the deeper knowledge in the molecular biology underlying this tumor. New immunotherapeutic targets have appeared recently trying to modulate the host immune response against the tumor. Furthermore, in the last three years, new targeted agents have changed the standard of care of other solid tumor types like renal cancer. We wonder if these new agents will be incorporated in the standard management of advanced melanoma patients in the coming years."
Source:http://www.cancer-therapy.org/CT7A/HTML/26._Blesa_et_al,_190-201.html
Treatment options for metastatic melanoma. A systematic review
Take care
Jimmy B
Accepted: 13 March 2009; electronically published: April 2009
Summary
"Metastatic melanoma is considered to be one of the most resistant tumors to standard chemotherapy approaches nowadays. Old anti-cancer treatments like dacarbacin (DTIC) or interleukin-2 (IL-2) continue to be the only approved treatments by the main worldwide health authorities. Up to now, no combination or new anti-targeted agent has shown an improvement in overall survival when compared to either of these two drugs alone. In fact, more than a dozen phase III randomized trials have tried to go beyond these old approaches, without meeting any success. Despite the fact that the median overall survival of patients diagnosed with metastatic melanoma is lower than 9 months, melanoma emerges as a challenging disease for testing new drugs and implementing the deeper knowledge in the molecular biology underlying this tumor. New immunotherapeutic targets have appeared recently trying to modulate the host immune response against the tumor. Furthermore, in the last three years, new targeted agents have changed the standard of care of other solid tumor types like renal cancer. We wonder if these new agents will be incorporated in the standard management of advanced melanoma patients in the coming years."
Source:http://www.cancer-therapy.org/CT7A/HTML/26._Blesa_et_al,_190-201.html
Treatment options for metastatic melanoma. A systematic review
Take care
Jimmy B
There is Enough Room for Novartis, Bristol Meyer Squibb and Pfizer for each to take part in the Melanoma Space Melanoma.. Jim Breitfeller
There is Enough Room for Novartis, Bristol Meyer Squibb and Pfizer for each to take part in the Melanoma Space.
With ASCO Annual meeting coming up at the end of May, I believe that there will be some excitement around monoclonal antibodies. In particular, anti-CTLA-4 blockage treatment will be under the spotlight. What will the overall survival rates look like? Well, speaking from my experience, anti-CTLA-4 has prolonged my life for over 27 months where as a stage IV Patient, I was given 6 to 9 months. This could not have happen with out the extra help from Interleukin -2.
See, once the CD4+ T-cells activated, they need to grow and cross-prime the CD8+ T-cells. While activated T-cells secretes IL-2 at a certain concentration to help promote proliferation of the CD4+ T-cells. If there is too much IL-2 at the beginning of the immune response, I believe that the ratio of CD4/CD8/CD3 would be altered causing
the Tregs (CD4+ CD25 fox P3) to gain the upper hand of suppression of the immune response. A subset of CD4 + cells called CD4 + CD25 + regulatory T (Treg) cells that expresses Forkhead box P3 (Fox P3).
With just adding Anti-CTLA-4 first, It has been reported that it suppresses the T regs and pushes the balance towards an immune response. Once the immune response is in progress, the CD4+ T-cell is needed to co-stimulate the CD8+ T-cell. A source of these cofactors for effective CD8+ T-cell stimulation can be provided by CD4+ T cells that release critical amounts of IL-2.
Once the CD8+ T-cell is activated, and is cultured in the presence of Interleukin 2, it results in the development of effector cells which are cytotoxic to tumor cells.
This is why we the patients need the Pharmacitical companies to work together. Each therapy will not work alone as a single agent. The response rate are between 10 and 22 percent for each therapy. If you do a sequential treatment with the proper dosage and timing, you will see a synergistic outcome.
“There are three parts of the equation in a clinical trial. There’s who has control, who gets the reward, and who takes the risk. Patients take all the risk, they have no control, and they get no reward. Patients ought to be the ones driving the process and get the reward out of it and have the control, since they are the ones that take the risk.”
Greg Simons
If we are taking all the risk, shouldn’t we have a say in our Destiny?
“We need to all work together for the common good of the Melanoma Patients”
“We need to take greed out of the equation and just do what is right for humanity”
Take care
Jimmy B
With ASCO Annual meeting coming up at the end of May, I believe that there will be some excitement around monoclonal antibodies. In particular, anti-CTLA-4 blockage treatment will be under the spotlight. What will the overall survival rates look like? Well, speaking from my experience, anti-CTLA-4 has prolonged my life for over 27 months where as a stage IV Patient, I was given 6 to 9 months. This could not have happen with out the extra help from Interleukin -2.
See, once the CD4+ T-cells activated, they need to grow and cross-prime the CD8+ T-cells. While activated T-cells secretes IL-2 at a certain concentration to help promote proliferation of the CD4+ T-cells. If there is too much IL-2 at the beginning of the immune response, I believe that the ratio of CD4/CD8/CD3 would be altered causing
the Tregs (CD4+ CD25 fox P3) to gain the upper hand of suppression of the immune response. A subset of CD4 + cells called CD4 + CD25 + regulatory T (Treg) cells that expresses Forkhead box P3 (Fox P3).
With just adding Anti-CTLA-4 first, It has been reported that it suppresses the T regs and pushes the balance towards an immune response. Once the immune response is in progress, the CD4+ T-cell is needed to co-stimulate the CD8+ T-cell. A source of these cofactors for effective CD8+ T-cell stimulation can be provided by CD4+ T cells that release critical amounts of IL-2.
Once the CD8+ T-cell is activated, and is cultured in the presence of Interleukin 2, it results in the development of effector cells which are cytotoxic to tumor cells.
This is why we the patients need the Pharmacitical companies to work together. Each therapy will not work alone as a single agent. The response rate are between 10 and 22 percent for each therapy. If you do a sequential treatment with the proper dosage and timing, you will see a synergistic outcome.
“There are three parts of the equation in a clinical trial. There’s who has control, who gets the reward, and who takes the risk. Patients take all the risk, they have no control, and they get no reward. Patients ought to be the ones driving the process and get the reward out of it and have the control, since they are the ones that take the risk.”
Greg Simons
If we are taking all the risk, shouldn’t we have a say in our Destiny?
“We need to all work together for the common good of the Melanoma Patients”
“We need to take greed out of the equation and just do what is right for humanity”
Take care
Jimmy B
Wednesday, May 6, 2009
Kurt's Story "The Battle with the Beast"
"I will try my best to impart Kurt's story to you.
Kurt was a healthy, 28 year old man living in Bloomington, MN. He was a night manager for the IHOP Restaurant located near the Mall Of America. He was one of nine children and grew up on a farm in southeastern MN. Even as a child he would much rather be in the house cleaning or cooking than doing the outside work. He was very modest and you didn't very often catch him without a shirt or only on a real hot day would he be found in a pair of shorts. He enjoyed playing softball and was on a couple of teams through the summer.
March 2008, Kurt's 92 year old grandmother was extremely ill in the hospital and in his haste to come to see her he slipped and fell in the shower which was in a tub. He hit on the edge of the tub with the left side armpit area. A month later he said it was still sore and he had a slight lump there. Kurt was a 6' 3", 210 lb. man. It was a hard fall and we assumed it was deeply bruised. The first week of May he went to a general doctor and she felt everything was fine on her examination. She thought that a lymph node may have been filled with fluid and to prevent an infection she wanted him to see a surgeon because they could possibly drain it. He saw the surgeon about 10 days later. They agreed with the first doctor. As they were checking things he noticed a mole on the right side of Kurt's back which had been there for at least 10 years or better and Kurt had not noticed any change in it. They did a punch biopsy. The Friday of Memorial Day weekend they called on the phone and told him it was Melanoma but not to worry because they got the whole spot out and they were sure it wasn't going to be a problem. They made an appointment for two weeks so they could check the lymph nodes and see what was happening. When that appointment came the swelling was worse. They decided to do a biopsy and it came back Melanoma. They then did a CT Neck, Chest, & Abd. Then they also did a PET Scan. The scans showed significant left supraclavicular and left axillary lymphadenopathy. A needle biopsy of a node showed metastatic melanoma. The Oncologist that he saw a Park Nicollett in Minneapolis said it was Stage 3 and the best treatment would be Interferon but it would be extremely harsh on the body.
Our daughter works at Mayo Clinic in Rochester. Kurt had also worked there one summer and one of the doctors that they both were associated with was very concerned and he talked with Dr. Markovic who was a personal friend of his. It was arranged for Kurt to see Dr. Markovic. Kurt also met with an ENT specialist. ENT said that the mass was too large and going under the clavicle so surgery was out of the question at that time because it was such a vascular area that was involved. At the appointment with Dr. Markovic he suggested the best thing was a trial using Avastin. Kurt opted for the trial. We had received material prior to Kurt's appointment from Dr. Markovic on melanoma and treatments and outcomes. I asked Dr. Markovic what stage he thought it was and what type. He said it didn't really matter because it was serious. Come to find out later, they immediately classified as stage 4. At this time, I still never found out what type. My concern was for the 8 other children in the family in case it was familial or genetic in nature.
Kurt immediately started chemotherapy the next day. They called it the BEAM Study. It was one day a week, every three weeks by IV. He would receive Taxol, Carboplatin, and either Avastin or a placebo. They did three treatments and then did another CT Chest, Abdomen, & Pelvis. The results showed that the disease was continuing to progress. They then suggested protocol N0675 which was a combination of Temozolomide and RAD001, and the Taxol and the Carboplatin in pill form. (He was not getting the Avastin on the BEAM Study.) This would continue for 7 weeks. At the end of the 7 weeks they did a CT again and found the disease still progressing and now it appeared the lung was involved. They then decided to go back to the first treatment but not in the study so they could be sure he was getting the Avastin. They also decided to do it once every week.
Kurt tolerated all of the treatments fairly well with minimal side effects. His arm was starting to really swell from the edema due to the lymphadenopathy though and that caused considerable pain. They could not get the pain down below a 7 on a 0-10 scale.
Right before Christmas they repeated the CT. Some of the lymphadenopathy had gone down but it appeared to have spread to the spine and the liver. They could not do a treatment that week because his platelets were too low. They would proceed with treatments the following week.
Kurt had shown them a spot down in the rectal area in November and they said it was a boil and would get better on its own. He showed them again in December and they weren't really concerned. In January it was draining and smelling. Around January 15 while he was having his chemo, Dr. Markovic came in and looked at it and decided to hospitalize him and have it lanced. Instead the surgeons took him to surgery and excised and biopsied it and it was melanoma. The surgeons got Kurt's hopes up because they thought they could go in and do surgery and reduce the mass in his chest and arm area. Upon examination they said there was no way. It was way to extensive. He could not continue with chemo until the surgery had totally healed. His hemoglobin was also very low so they had to transfuse 2 units of blood. When he went in to see the Doctor in February they still could not do chemo. By this time he was having tremendous problems with his arm and he was getting very unsteady. He was hospitalized again the middle of February due to the pain. They decided to try radiation and Kurt thought it was to reduce the mass so they then could do surgery. It was just to control the pain. They never did.
Kurt was hospitalized again in March due to a severe rash. They figure it was just the cancer manifesting itself. They then at that point informed him and our family that to continue with any treatment would be more harmful than it would help. They wanted him to agree to no resuscitation but he wouldn't. He still felt he was going to beat the beast. I was finally able to convince him that it was for the best. He was transferred to a nearby healt care facility on March 18. He was getting 60 mg of Methadone and 45 mg of gabapentin three times a day. He was getting 100 mg of morphine every hour and sometimes if they were doing some type of care it was given every 20 minutes. All of this never really did cut the pain below a 7. He was also given drugs to try and calm him down so that maybe he would accept that he was dying. He lasted abou 2 1/2 weeks in the health care center.
I feel that the doctors could have been a little more informative to him and our family. I am not saying they lied but if we didn't ask the question they weren't about to offer the idea or answer. Going through something like this you don't know what all you are suppose to be thinking about or asking. At the time they said they had done everything they could they said it was a very aggressive and fast moving melanoma but never have told us what type. Never have said that maybe the family should all be checked or be watchful or anything.
I believe that no matter what the outcome was going to be the same. I have no bitterness and I am thankful Kurt was able to have the expertise and care available to him that he did. He fought very hard. It was just not meant to be. He is now out of that pain and despair and for that I thank God daily.
Thanks for listening to Kurt's story. He had a tremendous birthday the other day, I am sure of it. I passed along your wishes."
Rhonda Graner
My heart goes out to the Graner Family.
Being on the frontline of this war, I sometimes become numb on what is going on around me and what we are fighting for. This story helps me focus on the task at hand. We need to find a therapy that at the very least, stops the progression of this terible disease. We all need to work together to find a cure.
Take care
Jimmy B
Kurt was a healthy, 28 year old man living in Bloomington, MN. He was a night manager for the IHOP Restaurant located near the Mall Of America. He was one of nine children and grew up on a farm in southeastern MN. Even as a child he would much rather be in the house cleaning or cooking than doing the outside work. He was very modest and you didn't very often catch him without a shirt or only on a real hot day would he be found in a pair of shorts. He enjoyed playing softball and was on a couple of teams through the summer.
March 2008, Kurt's 92 year old grandmother was extremely ill in the hospital and in his haste to come to see her he slipped and fell in the shower which was in a tub. He hit on the edge of the tub with the left side armpit area. A month later he said it was still sore and he had a slight lump there. Kurt was a 6' 3", 210 lb. man. It was a hard fall and we assumed it was deeply bruised. The first week of May he went to a general doctor and she felt everything was fine on her examination. She thought that a lymph node may have been filled with fluid and to prevent an infection she wanted him to see a surgeon because they could possibly drain it. He saw the surgeon about 10 days later. They agreed with the first doctor. As they were checking things he noticed a mole on the right side of Kurt's back which had been there for at least 10 years or better and Kurt had not noticed any change in it. They did a punch biopsy. The Friday of Memorial Day weekend they called on the phone and told him it was Melanoma but not to worry because they got the whole spot out and they were sure it wasn't going to be a problem. They made an appointment for two weeks so they could check the lymph nodes and see what was happening. When that appointment came the swelling was worse. They decided to do a biopsy and it came back Melanoma. They then did a CT Neck, Chest, & Abd. Then they also did a PET Scan. The scans showed significant left supraclavicular and left axillary lymphadenopathy. A needle biopsy of a node showed metastatic melanoma. The Oncologist that he saw a Park Nicollett in Minneapolis said it was Stage 3 and the best treatment would be Interferon but it would be extremely harsh on the body.
Our daughter works at Mayo Clinic in Rochester. Kurt had also worked there one summer and one of the doctors that they both were associated with was very concerned and he talked with Dr. Markovic who was a personal friend of his. It was arranged for Kurt to see Dr. Markovic. Kurt also met with an ENT specialist. ENT said that the mass was too large and going under the clavicle so surgery was out of the question at that time because it was such a vascular area that was involved. At the appointment with Dr. Markovic he suggested the best thing was a trial using Avastin. Kurt opted for the trial. We had received material prior to Kurt's appointment from Dr. Markovic on melanoma and treatments and outcomes. I asked Dr. Markovic what stage he thought it was and what type. He said it didn't really matter because it was serious. Come to find out later, they immediately classified as stage 4. At this time, I still never found out what type. My concern was for the 8 other children in the family in case it was familial or genetic in nature.
Kurt immediately started chemotherapy the next day. They called it the BEAM Study. It was one day a week, every three weeks by IV. He would receive Taxol, Carboplatin, and either Avastin or a placebo. They did three treatments and then did another CT Chest, Abdomen, & Pelvis. The results showed that the disease was continuing to progress. They then suggested protocol N0675 which was a combination of Temozolomide and RAD001, and the Taxol and the Carboplatin in pill form. (He was not getting the Avastin on the BEAM Study.) This would continue for 7 weeks. At the end of the 7 weeks they did a CT again and found the disease still progressing and now it appeared the lung was involved. They then decided to go back to the first treatment but not in the study so they could be sure he was getting the Avastin. They also decided to do it once every week.
Kurt tolerated all of the treatments fairly well with minimal side effects. His arm was starting to really swell from the edema due to the lymphadenopathy though and that caused considerable pain. They could not get the pain down below a 7 on a 0-10 scale.
Right before Christmas they repeated the CT. Some of the lymphadenopathy had gone down but it appeared to have spread to the spine and the liver. They could not do a treatment that week because his platelets were too low. They would proceed with treatments the following week.
Kurt had shown them a spot down in the rectal area in November and they said it was a boil and would get better on its own. He showed them again in December and they weren't really concerned. In January it was draining and smelling. Around January 15 while he was having his chemo, Dr. Markovic came in and looked at it and decided to hospitalize him and have it lanced. Instead the surgeons took him to surgery and excised and biopsied it and it was melanoma. The surgeons got Kurt's hopes up because they thought they could go in and do surgery and reduce the mass in his chest and arm area. Upon examination they said there was no way. It was way to extensive. He could not continue with chemo until the surgery had totally healed. His hemoglobin was also very low so they had to transfuse 2 units of blood. When he went in to see the Doctor in February they still could not do chemo. By this time he was having tremendous problems with his arm and he was getting very unsteady. He was hospitalized again the middle of February due to the pain. They decided to try radiation and Kurt thought it was to reduce the mass so they then could do surgery. It was just to control the pain. They never did.
Kurt was hospitalized again in March due to a severe rash. They figure it was just the cancer manifesting itself. They then at that point informed him and our family that to continue with any treatment would be more harmful than it would help. They wanted him to agree to no resuscitation but he wouldn't. He still felt he was going to beat the beast. I was finally able to convince him that it was for the best. He was transferred to a nearby healt care facility on March 18. He was getting 60 mg of Methadone and 45 mg of gabapentin three times a day. He was getting 100 mg of morphine every hour and sometimes if they were doing some type of care it was given every 20 minutes. All of this never really did cut the pain below a 7. He was also given drugs to try and calm him down so that maybe he would accept that he was dying. He lasted abou 2 1/2 weeks in the health care center.
I feel that the doctors could have been a little more informative to him and our family. I am not saying they lied but if we didn't ask the question they weren't about to offer the idea or answer. Going through something like this you don't know what all you are suppose to be thinking about or asking. At the time they said they had done everything they could they said it was a very aggressive and fast moving melanoma but never have told us what type. Never have said that maybe the family should all be checked or be watchful or anything.
I believe that no matter what the outcome was going to be the same. I have no bitterness and I am thankful Kurt was able to have the expertise and care available to him that he did. He fought very hard. It was just not meant to be. He is now out of that pain and despair and for that I thank God daily.
Thanks for listening to Kurt's story. He had a tremendous birthday the other day, I am sure of it. I passed along your wishes."
Rhonda Graner
My heart goes out to the Graner Family.
Being on the frontline of this war, I sometimes become numb on what is going on around me and what we are fighting for. This story helps me focus on the task at hand. We need to find a therapy that at the very least, stops the progression of this terible disease. We all need to work together to find a cure.
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
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