Medical Oncology
Kenneth G. Liu
Noah Kornblum
Non-Hodgkin Lymphoma <br /><br />
Andreas Kaubisch
<p>Gastro-Intestinal Cancer.</p>
Balazs Halmos
<p>Balazs Halmos, MD, MS was recruited in May 2015 to serve as Director of the Multidisciplinary Thoracic Oncology Program and Director of the Section of Thoracic Medical Oncology for Montefiore Health Systems. Dr. Halmos has also been appointed as the first Director of Clinical Cancer Genetics and Professor of Clinical Medicine at Einstein.</p>
<p>Dr. Halmos is an authority in the management of patients with malignancies of the thoracic cavity such as lung cancer, gastroesophageal cancer and thymoma. His research interests are focused on studies of targeted agents for the treatment of thoracic malignancies as well as translational studies aimed at different aspects of lung cancer biology such as oncogenic tyrosine kinase targeting, resistance to chemotherapy, radiation and targeted therapeutics. He will oversee the thoracic clinical trials program and spearhead the effort to develop guidelines for genetic testing for cancer patients of different anatomic sites to implement a personalized cancer medicine approach.</p>
<p>Dr. Halmos joined Montefiore and Einstein from Columbia University Medical Center, where he was Director of Thoracic Medical Oncology since 2009, Associate Professor of Medicine, and Chairman of the Cancer IRB. He completed a medical degree summa cum laude from Semmelweis University in Budapest, Hungary, an internal medicine residency at St.Luke’s-Roosevelt Hospital/Columbia University, and a hematology/oncology fellowship program at Beth Israel Deaconess Medical Center/Harvard Medical School, where he also obtained a master of science in clinical sciences from Harvard Medical School. Since completion of his fellowship, he has been on the faculties at Harvard, Case Western Reserve University, and Columbia.</p>
<p>Dr. Halmos is the recipient of multiple awards from organizations such as the American Society of Clinical Oncology, American Association for Cancer Research, and American Cancer Society and serves as a permanent review board member for the American Cancer Society. He is board certified in internal medicine and medical oncology.</p>
<p>Dr. Halmos is an authority in the management of patients with malignancies of the thoracic cavity such as lung cancer, gastroensophageal cancer and thymoma. His research interests are focused on studies of targeted agents for the treatment of thoracic malignancies as well as translational studies aimed at different aspects of lung cancer biology such as oncogenic tyrosine kinase targeting, resistance to chemotherapy, radiation and targeted therapeutics. He oversees the thoracic clinical trials program and spearheads the effort to develop guidelines for genetic testing for cancer patients of different anatomic sites to implement a personalized cancer medicine approach.</p>
Dr. Halmos is a thoracic medical oncologist focused on the management of patients with malignancies of the thoracic cavity, such as lung and gastroesophageal cancers as well as thymoma. He also oversees the thoracic clinical trials program of novel clinical studies at the Albert Einstein Cancer Center and is spearheading the effort to develop a molecular testing paradigm for cancer patients managed within the Montefiore Health System to facilitate a personalized cancer medicine approach throughout the health system.
Dr. Halmos’ research interests encompass clinical studies of experimental therapeutics, in particular studies of targeted agents for the treatment of thoracic malignancies as well as translational studies focused on different aspects of lung cancer biology, such as oncogenic tyrosine kinase targeting, resistance to chemotherapy, radiation and targeted therapeutics.
<p>Balazs Halmos, MD received his medical degree summa cum laude from Semmelweis University in Budapest, Hungary. He completed an internal medicine residency program at St.Luke’s-Roosevelt Hospital/Columbia University in New York City followed by a hematology/oncology fellowship program at Beth Israel Deaconess Medical Center/Harvard Medical School in Boston, Massaschuestts.</p><p>While in Dr. Halmos, also obtained an MS degree in Clinical Sciences from Harvard Medical School. Since completion of his fellowship, he has been a faculty member at Harvard, Case Western Reserve University and most recently an Associate Professor of Medicine at Columbia University Medical Center in New York. There he served as Director of Thoracic Oncology from 2009-2014 and was also Chair of the Cancer IRB.</p><p>Dr. Halmos also oversees the thoracic clinical trials program of novel clinical studies at the Montefiore Albert Einstein Cancer Center and is spearheading the effort to develop a molecular testing paradigm for cancer patients managed within the Montefiore to facilitate a personalized cancer medicine approach throughout the health system.</p><p>He is the recipient of multiple awards from prestigious organizations such as the American Society of Clinical Oncology, American Association for Cancer Research and the American Cancer Society, where he also serves as a permanent review board member. </p>
Rasim A. Gucalp
<p>Dr. Rasim Gucalp’s research interests include novel therapies in lung cancer as well as supportive care in cancer patients. He is actively involved in the multidisciplinary care of patients with lung cancer and central nervous system tumors. He is a member of several Montefiore Medical Center/Albert Einstein College of Medicine committees including the institutional tumor board, faculty senate, Pharmacy and Therapeutic Committee, and COGME.</p>
<p>A native of Turkey, Dr. Gucalp received his medical degree at Hacettepe University School of Medicine in Ankara, Turkey. After completing his medical residency at Downstate Medical Center in Brooklyn, he came to Montefiore Medical Center to complete his oncology fellowship. He is the director of the Hematology/Oncology Fellowship Program at Montefiore, and serves as a professor of Clinical Medicine at Albert Einstein College of Medicine. </p>
Kira Gritsman
<p><strong>The Roles of Signaling Pathways in Adult Blood Development and Leukemia</strong></p>
<p><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;">The Gritsman lab studies the signal transduction pathways that affect the early fate decisions of adult hematopoietic stem cells (HSCs) as they progress from an undifferentiated multipotent state to the generation of differentiated blood cells. When these early fate decisions go awry, this can lead to the formation of leukemia-initiating cells. We are interested in</span><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;"> how signaling pathways affect the self-renewal and differentiation of HSCs and malignant or pre-malignant stem cells in myeloid malignancies, such as acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and myeloproliferative neoplasms (MPN).</span></p>
<p><strong>Roles of the PI3 kinase isoforms in adult blood development</strong></p>
<p>PI3 kinase (PI3K) is a lipid kinase that is important for the regulation of metabolism, the cell cycle, apoptosis, and protein synthesis. In hematopoietic cells, there are four isoforms of the catalytic subunit of PI3K, each encoded by a separate gene. Emerging evidence suggests that these isoforms have unique functions in normal and cancer cells, but may substitute for each other in some contexts. We have generated a series of mouse knockout models that allow us to study the roles of each of these isoforms individually in adult hematopoiesis. For example, we have found that the p110alpha isoform is most important for red cell development, but is not required in normal blood stem cells. We have now also generated compound knockout mice to determine the redundant roles of the PI3K isoforms in blood development. We recently reported that PI3K isoforms play important redundant roles during the hematopoietic stress response, such as after chemotherapy. However, deletion of all 3 Class IA PI3K isoforms leads to a phenotype with impaired HSC differentiation, resembling myelodysplastic syndrome (MDS). We are studying how deletion of PI3K will impact normal HSC function, including self-renewal, proliferation, and differentiation along different blood lineages by affecting processes such as autophagy and epigenetic regulation in HSCs.</p>
<p><strong>Roles of the PI3 kinase isoforms in leukemia</strong></p>
<p>Acute myeloid leukemia (AML) is a genetically diverse disease, but activation of the PI3K pathway has been reported in up to 80% of cases. A subset of AML cell lines and AML patient samples respond to PI3K pathway inhibitors, but it is unclear how patients should be selected for potential response to these inhibitors. We found that RAS-mutated myeloid leukemias are particularly dependent on the p110alpha isoform of PI3K, and that pharmacologic inhibition of p110alpha can be used to treat both RAS-mutated cell lines and RAS-mutated leukemia in mice. Furthermore, we use cell lines, patient samples, and mouse models of leukemia to investigate the mechanisms of resistance to PI3K inhibition, with the goal of identifying new drug targets and designing new combination treatments for leukemia that incorporate PI3K inhibitors.</p>
<p><strong>RON Kinase in Myeloproliferative Neoplasms</strong></p>
<p>The myeloproliferative neoplasms (MPNs) are a group of diseases that are caused by kinase mutations in HSCs, which lead to uncontrolled proliferation of myeloid cells. The Philadelphia chromosome-negative MPNs are characterized by mutations in the JAK/STAT signaling pathway, and respond to JAK inhibitors, but resistance often develops. We recently discovered that the receptor Tyrosine kinase RON can physically interact with JAK2 in MPN cells, leading to potentiation of JAK/STAT signaling in resistant cells. Furthermore, we found that pharmacologic or genetic inactivation of RON can inhibit proliferation of MPN cells and re-sensitize resistant cells to JAK inhibitors.</p>
<p class="MsoNormal" style="margin: 0in 0in 0.0001pt; font-size: medium; font-family: 'Times New Roman', serif;"><strong><span style="font-size: 10.5pt; font-family: Verdana, sans-serif; color: #201f1e;">Member of the Cancer Dormancy and Tumor Microenvironment Institute </span></strong></p>
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<p class="MsoNormal" style="margin: 0in 0in 0.0001pt; font-size: medium; font-family: 'Times New Roman', serif;"><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;"> </span><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;">The Gritsman lab’s research interests include the contributions of signaling pathways to leukemic and pre-leukemic stem cell dormancy in minimal residual disease, which includes mechanisms of immune evasion. Furthermore, the Gritsman lab is interested in the roles of inflammatory signaling pathways and of the local microenvironment in bone marrow fibrosis, and in the evolution of myeloid neoplasms from the pre-malignant to malignant state. Our major goals are to identify opportunities for therapeutic targeting to prevent the transition from the pre-leukemic state to leukemia, or to eliminate minimal residual disease to prevent relapse.</span></p>
<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><a name="_GoBack"></a><span style="font-size: 11pt; font-family: Arial, sans-serif;">Ames, K., <sup> </sup>Kaur,<sup> </sup>I., Shi, Y., Tong, M., Sinclair, T., Hemmati, S., Glushakow-Smith, S.G., Tein, E., Gurska, L., Steidl, U., Dubin, R., Shan, J., Montagna, C., Pradhan, K., Verma, A., and <strong><u>Gritsman, K.</u></strong>, Deletion of PI3-Kinase Promotes Myelodysplasia Through Dysregulation of Autophagy in Hematopoietic Stem Cells, <strong><em>Science Advances</em></strong><em> 2023. </em>doi: <a href="https://nam04.safelinks.protection.outlook.com/?url=https%3A%2F%2Fdoi.o…; target="_blank" rel="noopener"><span style="color: black; text-decoration: none;">10.1126/sciadv.ade8222</span></a><u>, </u>PMID: 36812307</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Folgado Marco, V., Ames, K., Chuen, J., <strong><u>Gritsman, K.</u></strong> & Baker, N., Haploinsufficiency of the essential gene <em>RpS12</em> causes defects in erythropoiesis and hematopoietic stem cell maintenance, <em> <strong>eLife</strong> </em>2023 Jun 5;12:e69322. doi: 10.7554/eLife.69322. PMID: 37272618</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Gurska, L.M., Okabe, R., Schurer, A., Tong, M.M., Soto, M., Choi, D., Ames, K., Glushakow-Smith, S., Montoya, A., Tein, E., Miles, L.A., Cheng, H., Hankey-Giblin, P., Levine, R.L., Goel, S., Halmos, B., and <strong><u>Gritsman, K.</u></strong> Crizotinib has Preclinical Efficacy in Philadelphia-negative Myeloproliferative Neoplasms, <strong><em>Clinical Cancer Research</em></strong> 2022 Dec 20:CCR-22-1763. doi: 10.1158/1078-0432.CCR-22-1763. PMID: 36537918</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Gurska, L., Ames, K., and <strong><u>Gritsman, K</u></strong>, Signaling Pathways in Leukemic Stem Cells, </span><span style="font-size: 11pt; font-family: Arial, sans-serif; color: #333333; letter-spacing: 0.2pt; background-color: #fcfcfc;">In: Zhang H., Li S. (eds) Leukemia Stem Cells in Hematologic Malignancies. <strong>Advances in Experimental Medicine and Biology</strong>, vol 1143. Springer, Singapore</span><span style="font-size: 11pt; font-family: Arial, sans-serif;">, July 24, 2019, doi: <a href="https://doi.org/10.1007/978-981-13-7342-8_1"><span style="color: black; letter-spacing: 0.2pt; background-color: #fcfcfc; text-decoration: none;">https://doi.org/10.1007/978-981-13-7342-8_1</span></a><span style="letter-spacing: 0.2pt; background-color: #fcfcfc;">; </span>PMID: 31338813, PMCID: <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/pmc7249489/" target="_blank" rel="noopener"><span style="color: black; text-decoration: none;">PMC7249489</span></a></span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Hemmati, S., Sinclair, T., Tong, M., Bartholdy, B., Okabe, R.O., Ames, K., Ostrodka, L., Haque, T., Kaur, I., Mills, T. S., Agarwal, A., Pietras, E.M., Zhao, J.J., Roberts, T.M., and <strong><u>Gritsman, K.</u></strong>, PI3 kinase alpha and delta promote hematopoietic stem cell activation, <strong><em>JCI Insight </em></strong>2019 doi.org/10.1172/jci.insight.125832</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Mitchell, K., Barreyro, L., Todorova, T., Taylor, S., Antony-Debre, I., Narayanagari, S., Carvajal, L., Leite, J., Piperdi, Z., Pendurti, G., Mantzaris, I., Paietta, E., Verma, A., <strong><u>Gritsman, K., </u></strong>and Steidl, U. IL1RAP potentiates multiple oncogenic signaling pathways in AML, <strong><em>Journal of Experimental Medicine</em></strong><em>. </em>2018 May 17. doi: 10.1084/jem.20180147, PMID: 29773641</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Hemmati, S., Haque, T., and <strong><u>Gritsman, K</u>, </strong>Inflammatory Signaling Pathways in Pre-leukemic and Leukemic Stem Cells, <strong><em>Frontiers in Oncology</em></strong><em> </em>2017 Nov 13;7:265. doi: 10.3389/fonc.2017.00265</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Bhagat, T.D., Chen, S., Bartenstein, M., Barlowe, A.T., Von Ahrens, D., Choudhary, G.S., Tivnan, P., Amin, E., Marcondes, M., Sanders, M.A., Hoogenboezem, R.M., Kambhampati, S., Ramanchandra, N., Mantzaris, I., Sukrithan, V., Laurence, R., Lopez, R. Bhagat, P., Giricz, O., Sohal, D., Wickrema, A., Yeung, C., <strong><u>Gritsman, K.,</u></strong> Aplan, P., Hochedlinger, K., Yu, Y., Pradhan, K., Zhang, J., Greally, J.M., Mukherjee, S., Pellagatti, A., Boultwood, J., Will, B., Steidl, U., Raaijmakers, M.H.G.P., Deeg, H.J., Kharas, M.G. and Verma, A. Epigenetically Aberrant Stroma in MDS Propagates Disease Via Wnt/b-Catenin Activation, 2017 <strong><em>Cancer Research</em></strong> 2017 Jul 6. pii: canres.0282.2017. doi: 10.1158/0008-5472</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Yuzugullu, H., Baitsch, L., Von, T., Steiner, A., Tong, H., Ni, J., Clayton, L., Bronson, R., Roberts, T., <strong><u>Gritsman, K</u></strong><u>.</u>, and Zhao, J.J. A p110b-Rac signaling loop mediates Pten-loss-induced perturbation of hematopoiesis and leukemogenesis. <strong><em>Nature Communication</em></strong><em>s </em>October 7,2015, doi:10.1038/NCOMMS9501</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Yoda, A., Adelmant, G., Tamburini, J., Chapuy, B., Shindoh, N., Yoda, Y., Weigert, O., Kopp, N., Wu, S-C., Kim, S., Liu, H., Tivey, T., Christie, A.L., <strong><u>Gritsman, K.</u></strong>, Gotlib, J., Deininger, M., Turley, S., Tyner, J., Marto, J., Weinstock, D.M., and Lane, A.A. Mutations in G-protein beta subunits promote transformation and kinase inhibitor resistance <strong><em>Nature Medicine</em></strong><em> </em>2015 (1):71-5.</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><strong><u><span style="font-size: 11pt; font-family: Arial, sans-serif;">Gritsman, K</span></u></strong><strong><span style="font-size: 11pt; font-family: Arial, sans-serif;">.</span></strong><span style="font-size: 11pt; font-family: Arial, sans-serif;">, Yuzugullu, H., Von, T., Yan, H., Clayton, L., Fritsch, C., Maira, S.-M., Hollingworth, G., Choi, C., Khandan, T., Paktinat, M., Okabe, R.O., Roberts, T.M., and Zhao, J.J. Hematopoiesis and RAS-driven myeloid leukemia differentially require PI3K isoform p110alpha<strong>. <em>Journal of Clinical Investigation </em></strong>2014;124(4):1794–1809. http://www.jci.org/articles/view/69927</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Kharas, M.G. and <strong><u>Gritsman, K</u></strong>. Akt: A Double-Edged Sword for Hematopoietic Stem Cells. <strong><em>Cell Cycle</em> </strong>2010; Vol 9; Issue 7</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Kharas, M.G., Okabe, R., Ganis, J.J., Gozo,M., Khandan,T., Paktinat, M., Gilliland, D.G., and <strong><u>Gritsman, K</u>.</strong> Constitutively Active AKT Depletes Hematopoietic Stem Cells and Induces Leukemia in Mice. <strong><em>Blood </em></strong>2010; 115(7): 140615 http://www.bloodjournal.org/content/115/7/1406</span></p>
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Mendel Goldfinger
<p>Dr. William Osler famously said, “The good physician treats the disease; the great physician treats the patient who has the disease.” I am a strong believer in individualizing treatment plans unique to each patient based on understanding the patient as a whole and the specifics of their disease. I am committed to each patient’s care and work hard to ensure that every single patient has the most positive clinical outcome.</p>
<p>I primarily treat people with hematologic malignancies such as Lymphoma, Multiple Myeloma, Leukemia and Bone Marrow diseases. I have a special interest in Chimeric Antigen Receptor T-cell Therapy (CAR T-cell), stem cell transplantation and the use of antibodies to fight cancer. My research focus is in developing novel cellular immunotherapies to target cancer cell antigens. I work with colleagues in our basic science laboratories to discover innovative ways to stimulate an individual patient’s immune system to fight cancer and research how to enhance their tumor’s immune microenvironment to make their cancer cells more susceptible to immunotherapy. I also have an interest in chemotherapeutic pharmacology and understanding how to precisely target each patient’s tumor. Every patient’s regimen is tailored by identifying and targeting the tumor’s mutation and delivering a therapy based on a precision medicine approach.</p>
<p>I am passionate about giving every patient access to world-class heme malignancies care. The challenge is that some of our best therapies are only available at tertiary level cancer centers like Montefiore which is a long-distance travel for many patients. At the same time, patients benefit from getting their cancer care close to home, in their own community. As director of the Montefiore Hematologic-Malignancy Network, I have worked with our heme malignancy team to develop a Co—Management Model, where we collaborate with community medical oncologists to enable patients who live far from the Bronx access to novel therapies only available at an NCI designated Cancer Center.</p>
Swati Goel
<p>Dr. Swati Goel is an Assistant Professor of Medicine (Hematology). She completed medical school education at the All India Institute of Medical Sciences and finished postgraduate hematology-oncology training at NYU Langone Medical Center.</p>
<p>Dr. Goel sees patients with blood disorders and blood-related cancers. She specializes in the field of myeloproliferative disorders like myelofibrosis, polycythemia vera, and essential thrombocytosis. She is the leader of Myeloproliferative Disorder Clinic at Montefiore Einstein.</p>
Myeloproliferative neoplasms, and the conditions she treats include myelofibrosis, polycythemia vera, essential thrombocythemia, mastocytosis, eosinophilia, anemia and pancytopenia.
Myeloproliferative neoplasms
<p>Swati Goel, MBBS, is Leader of the Myeloproliferative Disorder Clinic, Assistant Director of the Hematology-Oncology Fellowship Program and Associate Professor in the Department of Oncology and Medicine at Montefiore Einstein. Her area of clinical focus is myeloproliferative neoplasms, and the conditions she treats include myelofibrosis, polycythemia vera, essential thrombocythemia, mastocytosis, eosinophilia, anemia and pancytopenia.</p><p>After earning her Bachelor of Medicine, Bachelor of Surgery from the All-India Institute of Medical Sciences in New Delhi, India in 2006, Dr. Goel completed her residency in internal medicine at Montefiore Einstein in 2010. Afterward, she underwent a hematology-oncology fellowship at New York University School of Medicine, completing it in 2013.</p><p>Dr. Goel’s research focus is myeloproliferative neoplasms. She is the principal investigator in many clinical trials involving myelofibrosis, polycythemia vera and essential thrombocythemia, and her work has been published in numerous peer-reviewed journals, articles and abstracts.</p><p>Dr. Goel is board certified in Internal Medicine, Medical Oncology and Hematology. She is a member of the American Society of Hematology and the American Society of Clinical Oncology. She is also the Clinical Competency Committee Leader and Program Evaluation Committee Member for the Hematology-Oncology Fellowship at Montefiore Einstein. In 2012, Dr. Goel won the Abstract Achievement Award for oral presentation at the American Society of Hematology Annual Meeting.</p>
Benjamin A. Gartrell
Dr. Gartrell's clinical focus has been on treating genitourinary malignancies including prostate cancer, bladder cancer, renal cell cancer, and testicular cancer.
With a vast range of research interests, Dr. Gartrell focuses on translational research evaluating the significance of a novel immune checkpoint molecule in bladder cancer, evaluating the role of the autonomic nervous system in prostate cancer, toxicities associated with anticancer therapies, and the impact of bone metastasis on patients with prostate cancer.
<p>Benjamin A. Gartrell, MD, is Director, Genitourinary Malignancy Program at Montefiore and an Assistant Professor of Oncology and Urology at our Albert Einstein College of Medicine. Since joining the Montefiore team in 2012, his expertise has been in treating genitourinary malignancies including prostate cancer, bladder cancer, renal cell cancer, and testicular cancer. He is also very active in translating science findings in collaboration with research colleagues at Einstein. </p><p>In 2000, Dr. Gartrell received his Bachelor of Arts in Chemistry at the College of Wooster in Ohio. Following this, he attended the Northwestern University?s Feinberg School of Medicine, in Chicago, Illinois, where he received his Doctor of Medicine in 2005. His postgraduate training began in 2005 with an internship and residency in Internal Medicine at Case Western Reserve University, which he completed in 2008. He then completed a fellowship in Hematology/Oncology at Mount Sinai School of Medicine in 2012 and became Chief Fellow from 2010-2011. </p><p>With a vast range of research interests, Dr. Gartrell focuses on translational research evaluating the significance of a novel immune checkpoint molecule in bladder cancer, evaluating the role of the autonomic nervous system in?prostate cancer, toxicities associated with anticancer therapies, and the impact of bone metastasis on patients with prostate cancer. His work has been published in a number of peer-reviewed journals, including the Journal of Clinical Oncology, Urologic Oncology, and European Urology. Dr. Gartrell also participates in community outreach to promote Prostate Cancer Awareness.</p><p>In 2015, Dr. Gartrell received Most Outstanding Faculty Educator, selected by the graduating oncology fellows at our Albert Einstein College of Medicine. He is also a recipient of the Paul Calabresi Career Development Award for Clinical Oncology (PCACO). He is board certified by the American Board of Internal Medicine in Medical Oncology and Hematology, and is a member of the American Society of Clinical Oncology. </p>