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Robert Fine, MD
RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified) )| Communities: Pancreatic Cancer , Colon and Rectal Cancer , Stomach Cancer , Esophagus Cancer , Liver and Intraheptic Cancer | Answers: 8 |
| Member Since: Jun. 2012 |
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Professional Statement
Robert L. Fine, M.D., is the Herbert Irving Associate Professor of Medicine and Director of Experimental Therapeutics at the Herbert Irving Comprehensive Cancer Center, New York Presbyterian Hospital-Columbia University Medical Center. Dr. Fine specializes in caring for patients with pancreatic cancer, neuroendocrine cancers, untreatable tumors and brain tumors. His expertise lies in creating new experimental therapies for his laboratory and translating them directly to the clinic population. Dr. Fine received his B.A. and B.S. degrees in Philosophy and BioChemistry and finished medical school at the University of Chicago Pritzker School of Medicine where he graduated with research honors. He conducted his internal medicine training at Stanford University Hospital and did a medical oncology fellowship at the National Cancer Institute, National Institutes of Health, where he stayed on faculty for an additional three years in experimental pharmacology. He then spent six years at Duke University Cancer Center as an Assistant Professor of Medicine before coming to Columbia in 1996.
Dr. Fine is involved in clinical and experimental research in the following solid tumors: pancreatic cancer, neuroendocrine cancers, untreatable tumors and brain tumors. He currently runs seven investigator-initiated clinical trials in GI and neuroendocrine tumor studies. In addition, his laboratory with three Ph.D. postdoctoral fellows have developed a new gene therapy for pancreatic cancer and a P53 peptide therapy for mutant P53 cancers, which have been patented and hold great promise as new treatments for cancer. Additionally, he has developed two separate novel treatments for pancreatic cancer that are currently being tested in the clinic. Preliminary results for the GTX study show higher response and survival rates than any other study published as well as the highest successful conversion rate of inoperable pancreatic cancer into operable status. He has published 105 peer-reviewed articles, 220 abstracts, and 18 book chapters. Recently, Dr. Fine was chosen by his peers as one of the top three thought leaders in pancreatic cancer, and has been listed for the past three years in New York Magazine as one of the top doctors in his field.
Dr. Fine is involved in clinical and experimental research in the following solid tumors: pancreatic cancer, neuroendocrine cancers, untreatable tumors and brain tumors. He currently runs seven investigator-initiated clinical trials in GI and neuroendocrine tumor studies. In addition, his laboratory with three Ph.D. postdoctoral fellows have developed a new gene therapy for pancreatic cancer and a P53 peptide therapy for mutant P53 cancers, which have been patented and hold great promise as new treatments for cancer. Additionally, he has developed two separate novel treatments for pancreatic cancer that are currently being tested in the clinic. Preliminary results for the GTX study show higher response and survival rates than any other study published as well as the highest successful conversion rate of inoperable pancreatic cancer into operable status. He has published 105 peer-reviewed articles, 220 abstracts, and 18 book chapters. Recently, Dr. Fine was chosen by his peers as one of the top three thought leaders in pancreatic cancer, and has been listed for the past three years in New York Magazine as one of the top doctors in his field.
Professional Info
Credential: MD
Primary specialty: Oncology - Hematology/Oncology
Medical school: University of Chicago Pritzker School of Medicine
Residency: Stanford University Hospital
Internship: Stanford University Hospital
Fellowship: National Cancer Institute
Hospital affiliation: New York Presbyterian Hospital-Columbia University Medical Center
Practice address:
Irving Pavilion 10 161 Fort Washington Ave at W 165th St.
New York, NY
Practice phone number: (212) 305-5098
RobertFineMD Activities
Having BRCA mutation definitely increases your chance for developing pancreatic, breast, ovarian, and prostate cancers at a young age (under 60 years). The BRCA mutations are found mainly in Ashkenazi Jews, Scandinavians, Irish, and UK peoples. BRCA2 mutations are generally associated with a much higher incidence of pancreatic, ovarian, and breast cancers while BRCA1 mutations are more associated with breast, ovarian, and prostate cancers. However, in our patients at Columbia University Medical Center where we study BRCA mutations, we have found almost a 50/50 split amongst patients with BRCA1 and BRCA 2 mutations with pancreatic cancer. There are no differences between BRCA1 and 2 response rates, but there are definitely improved response rates in BRCA mutant patients to DNA alkylating agents, topoisomerase 1 or 2 agents, and PARP inhibitors.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
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9 months ago
Chemoradiation should be used only in patients with inoperable, non-metastatic pancreatic cancer because of arterial or venous involvement by tumor. The chemoradiation treatment traditionally can convert 15% of patients to operable status by shrinking the tumor away from the blood vessels. In two previous studies of neoadjuvant GTX at our institution, we have had successfully converted 67% and 62% of patients from inoperable to operable status.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
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Answer |
9 months ago
Tarceva (erlotinib) has been studied in metastatic pancreatic cancer patients. It leads to a minimal two week prolongation of survival over Gemzar alone. Because this disease has so few treatment options, the FDA approved the drug. I believe the reason that it has such low efficacy in pancreatic tumors is because the EGF receptor is not mutated like it is in lung cancer, for instance. The majority of times the K-ras, which is one step below EGFR, is constitutively mutated/turned on to signal the cell to grow. Therefore, the Tarceva inhibits one step above the mutation which is why it doesn’t work in the majority of pancreatic cancer patients. However, we have found that it does work well in patients with wild type, or normal, K-ras. Having wild type K-ras means that if you turn off the EGFR signal above it, you inhibit the pathway because K-ras is not turned on or mutated. Patients on Tarceva that will respond generally develop a rash on their face, which is a biomarker for a response but it has nothing to do with the anti-tumor effect.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
1
Answer |
9 months ago
K-ras is a very important oncogene that, as with all oncogenes, is essential for development of the normal fetus. These genes were called proto-oncogenes and, when they became mutated, they became cancer causing oncogenes. So in essence, cancer is an attempt by our body to redevelop fetal tissue. The problem is that it doesn’t know how to stop growing because the brakes are impaired. The normal K-ras gene is vital for the development of normal fetal tissue and organs but when it becomes mutated it tries to make new fetal tissue (cancer) but doesn’t know how to shut off.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
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9 months ago
MAPK stands for mitogen activated protein kinase. Ninety-five percent of pancreatic cancer patients have mutated Ras with normal or amplified EGFR (epidermal growth factor receptor). This mutation of Ras is in the MAPK pathway which drives the tumor to grow and prevents the cell from dying by signaling through the MAPK pathway. It is very vital, therefore, to the majority of patients with pancreatic cancer that the MAPK pathway be targeted. The GTX regimen was developed in our lab with this in mind as it specifically inhibits the MAPK-MEK phosphorylation signaling step. We believe that this is why it is so effective.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
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9 months ago
Again, that depends upon the performance status of the patient. If the patient has maintained a good performance status (PS 0, 1, or 2) then a second line therapy is certainly possible. There are multiple second line treatments such as GTX, OFF, or Gemzar alone.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
1
Answer |
9 months ago
The most important factor that determines treatment direction is the patient’s performance status. If the patient is doing everything that they normally do, such as working, and have very little weight loss, then they can be treated with more aggressive regimens which prolong survival substantially. If they have a greater than 20 pound weight loss, or poor performance status, then the best treatment would be gemcitabine alone.
It is important to express to the oncologist what you want—whether that is chemotherapy, aggressive therapy, or best supportive care. It is also important to discuss your religious background and beliefs so that he/she can make a better informed decision as to what is the best therapy for you.
It is important to express to the oncologist what you want—whether that is chemotherapy, aggressive therapy, or best supportive care. It is also important to discuss your religious background and beliefs so that he/she can make a better informed decision as to what is the best therapy for you.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
1
Answer |
9 months ago
The physician will interview the patient, do a physical exam, and review the data. The oncologist will make a decision as to what is the best therapy for that patient with their current stage of cancer. Unfortunately, only 15% of patients with pancreatic cancer present with operable disease and are able to get a Whipple surgery. However, even if you have a Whipple, the relapse rates post-operatively are 80%. Therefore, post-operative chemotherapy is vital. In an ongoing, prospective, phase II trial of GTX adjuvant (or post-operative) chemotherapy, we have seen a decrease from 80% to 25% relapse rate at 18 months post-surgery.
Another important reminder for your first appointment is to bring a list of questions for the oncologist to answer. Note your changes in appetite, weight, color of urine and stool, and if you have pain, make sure the physician knows.
Another important reminder for your first appointment is to bring a list of questions for the oncologist to answer. Note your changes in appetite, weight, color of urine and stool, and if you have pain, make sure the physician knows.
New answer by RobertFineMD (Physician - Oncology - Hematology/Oncology (Verified))
1
Answer |
9 months ago
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