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Jeffrey Weber, MD, PhD
JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified) )| Communities: Melanoma (Cutaneous) | Answers: 8 |
| Member Since: May. 2012 |
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Professional Statement
Jeffrey S. Weber, M.D., Ph.D., is the director of the Donald A. Adam Comprehensive Melanoma Research Center at Moffitt Cancer Center, with the charge of bringing together basic scientists, clinical and translational investigators and prevention/epidemiology scientists in an integrated overall melanoma research effort that rapidly brings new drugs and ideas to the clinic. Weber has an extensive history of conducting translational and investigator-initiated clinical trials. Dr. Weber is also a professor of Oncology and Medicine at the University of South Florida College of Medicine.
Dr. Weber received his doctorate in Molecular Cell Biology from Rockefeller University. He received his medical degree from New York University Medical Center. He then completed an internship and residency in Medicine at the University of California. Dr. Weber also trained at the National Cancer Institute.
Dr. Weber’s research interests lie in the monitoring and characterization of T cell responses to vaccination in cancer patients, and in the establishment of in vitro models to facilitate the understanding of how immune modulating antibodies amplify T cell responses in patients. He is also interested in the mechanisms by which achieving autoimmunity induces regression of cancer.
Dr. Weber received his doctorate in Molecular Cell Biology from Rockefeller University. He received his medical degree from New York University Medical Center. He then completed an internship and residency in Medicine at the University of California. Dr. Weber also trained at the National Cancer Institute.
Dr. Weber’s research interests lie in the monitoring and characterization of T cell responses to vaccination in cancer patients, and in the establishment of in vitro models to facilitate the understanding of how immune modulating antibodies amplify T cell responses in patients. He is also interested in the mechanisms by which achieving autoimmunity induces regression of cancer.
Professional Info
Credential: MD
Primary specialty: Oncology - Hematology/Oncology
Medical school: New York University Medical Center
Residency: University of California
Fellowship: National Cancer Institute
Areas of expertise: Immunotherapy of melanoma and other malignancies, with a focus on vaccines, adoptive immunotherapy, dendritic cell therapy and the use of immune modulating antibodies.
Hospital affiliation: Moffitt Cancer Center
Practice address:
12902 Magnolia Drive
Tampa, FL
33612
Practice phone number: 813-745-1968
JeffreyWeberMDPhD Activities
If you have already started an adjuvant therapy for your stage IIIA melanoma, and you are tolerating the drug, I would stick with it. There are no new FDA approved adjuvant therapies than standard interferon and PEG-interferon at this time. Trials for resected stage IIIA melanoma are few, and the recent ipilimumab versus placebo trial is finished with accrual and in the follow-up phase. The current US intergroup trial of ipilimumab versus high dose interferon is a 1500 patient trial that is in the middle of accrual, but does not include stage IIIA patients. The GSK MAGE-3 adjuvant trial has closed to accrual and is also in the follow-up phase. New trials are soon to open with vemurafenib in BRAF mutated stage III patients, but that is in the future. I would keep track of the melanoma news at the major meetings, of which there is an increasing number, line the Society for Melanoma Research meeting and the Melanoma Centers meeting each November, the Paris Melanoma meeting in April, the New York melanoma meeting in March, the European Society for Medical Oncology meeting in late September, and the ASCO meeting in June.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
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10 months ago
If CT-011 development is abandoned, there will still be other drugs that are similar in development, such as BMS 936558, which is very promising, and which you have read about at our recent ASCO meeting in Chicago; AMP-224, co-developed by GSK and Amplimmune; a PD-L1 antibody from Genentech, a PD-L1 antibody from BMS; there is the Merck PD-1 antibody MK_3475 that is actively in testing; and finally there is another PD-1 antibody from Novartis. Having had one of those, including CT-011, will likely exclude patients from receiving another such drug in a trial.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
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10 months ago
Nobody has any good information about how long the PD-1 antibodies work after the treatment has stopped, but my guess would be that they will work for many months after stopping. In our current trials at Moffitt, treatment is called for over a period of 30 months, and we do not know that a longer period of time is better. In the phase I-II trial presented at ASCO by Dr. Stephen Hodi, there were patients still in partial or complete remission well over 2 years from starting therapy, even though the drug was stopped just short of 2 years.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
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10 months ago
The latest news about resistance to BRAF inhibitors is that there are many different pathways by which the tumor may evade these drugs. There are three different means by which the resistance occurs. Think of the growth pathway for melanoma to be like a river flowing along, and there are various cities along the river with locks like the Panama Canal that a boat must pass to continue the journey and cause the tumor to grow. There may be mutations in the upstream molecule RAS, which causes the lock to stay open upstream of the BRAF lock, causing more water to flow along past BRAF; there may be a new canal that developed, bypassing the BRAF lock, allowing the water to move around the river and flow from the beginning past BRAF and beyond it, rejoining the river later. A gene called COT may be increased in some melanomas, causing this to happen. Finally, a whole new pathway, complete with its own river and its own locks may develop quickly, totally bypassing the entire MAP kinase pathway or river that BRAF is a part of. The new parallel river is the Akt pathway, promoted by PDGF receptor binding. Most patients that receive BRAF inhibitors eventually develop resistance to those agents, although a fair number of patients may stay on the drug and derive benefit for years.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
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10 months ago
If the melanoma is one of the 50% or so that have a BRAF mutation that usually means it is a so-called “driver” mutation, by which we mean the melanoma cell becomes dependent on the mutated BRAF protein for its uncontrolled growth and spread. Patients with that mutation have a slightly worse outcome than those that do not, and those with the mutation may be a bit younger than those without it. The most important implication for a patient that has a BRAF mutated melanoma is that there are now a number of drugs that specifically inhibit and block the mutated BRAF, resulting in rapid and impressive shrinkage of tumors. The first of those drugs, vemurafenib, was approved by the FDA in August 2011 for patients with metastatic melanoma, and is a very effective drug. Several other drugs are also being developed that inhibit mutated BRAF and may get approved by the FDA in coming years. Vemurafenib prolongs survival in patients that have had no prior treatment for their melanoma, compared to chemotherapy alone, and its approval is a major milestone in the melanoma field.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
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10 months ago
Ipilimumab binds very strongly to a molecule on T cells called CTLA-4, which blocks it from binding to another molecule on other immune cells that acts as a brake on immune activation. In doing this the ipilimumab cuts the “brake cable” on the immune system and allows the immune killing cells that could attack tumors to do their job in an unfettered manner, freeing them up to destroy tumors. In doing so, it cuts the brake cable, but the immune cells now have a slightly hard time “stopping” and coming to a halt, so the flip side of cutting the immune brake is too much immunity which we see manifested as the immune related side effects of ipilimumab discussed in this answer -http://talkabouthealth.com/when-a-patient-is-taking-ipilimumab-what-side-effects-do-you-tell-the-patients-to-watch-for-in-particular-and-how-do-you-prepare-them.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
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10 months ago
The key to management of side effects from ipilimumab is good communication between providers and patient. We tell patients to call for diarrhea more than one in a 24 hour period, for fevers of greater than 100.5 Fahrenheit, severe and profound fatigue, and any bloody bowel movements. We make clear what the spectrum of side effects is, starting with the rashes and itchiness that are most common, then describing the endocrine side effects generally presenting with fatigue, and finally the diarrhea and colitis, which are the most morbid side effects. All patients starting ipilimumab get a prescription for lomotil , and are told not to fill it until they speak with us on the phone if there is diarrhea. We also make it clear that any severe abdominal pain, nausea or vomiting or profound rash over 50% of the body or more merit a phone call.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
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10 months ago
We usually will use CT scans of the chest, abdomen and pelvis to gauge how much tumors have shrunk. We literally use a computer cursor to measure the dimensions of at least the 5 biggest and most obvious tumors and decide how much the total burden of tumors that can be measured have shrunk. WE also do MRI scans of the brain to measure lesions in the brain the same way. Sometimes we measure just the longest dimension of a tumor, sometimes the cross sectional product of the two longest dimensions.
New answer by JeffreyWeberMDPhD (Physician - Oncology - Hematology/Oncology (Verified))
1
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10 months ago
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