Mark A. Ramirez

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Mark

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Ramirez

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1467494336

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3064

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Stuart Packer

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Stuart

Last Name

Packer

NPI

1124059621

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13484

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<p>Stuart Packer, MD, is a medical oncologist with extensive experience in treating lung, head and neck, prostate and other types of cancer. After graduating magna cum laude from Case Western Reserve University, Dr. Packer received his medical degree from the State University of New York/Downstate Medical Center. He went on to complete a residency in medicine and fellowship in hematology/medical oncology at Duke University Medical Center. Since then Dr. Packer has held clinical and teaching positions at leading cancer centers, including Memorial Sloan-Kettering Cancer Center, Mount Sinai School of Medicine and Montefiore Einstein Center for Cancer Care.</p>
<p>Dr. Packer&rsquo;s clinical expertise is in medical management of lung cancer, head and neck cancer and prostate cancer. He is director of the melanoma and sarcoma programs at Montefiore Einstein Center for Cancer Care. In addition, Dr. Packer is medical director of Montefiore&rsquo;s Oncology Care Model (OCM), an alternative payment model sponsored by the Centers for Medicare and Medicaid Services and aimed at improving patient care coordination and appropriateness of care.</p>
<p>Dr. Packer is the author or co-author of medical textbook chapter and articles in peer-reviewed journals, including <em>Cancer, Clinical Cancer Research, British Medical Journal</em> and <em>Lung Cancer</em>. He is a member of the American Society of Clinical Oncology and the American Society of Hematology.</p>

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Dr. Packer&rsquo;s clinical expertise is in medical management of lung cancer, head and neck cancer and prostate cancer.

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5497

Biography

<p>Stuart Packer, MD, is a medical oncologist with extensive experience in treating lung, head and neck, prostate and other types of cancer. After graduating magna cum laude from Case Western Reserve University, Dr. Packer received his medical degree from the State University of New York/Downstate Medical Center. He went on to complete a residency in medicine and fellowship in hematology/medical oncology at Duke University Medical Center. Since then Dr. Packer has held clinical and teaching positions at leading cancer centers, including Memorial Sloan-Kettering Cancer Center, Mount Sinai School of Medicine and Montefiore Einstein Center for Cancer Care.</p><p>Dr. Packer&rsquo;s clinical expertise is in medical management of lung cancer, head and neck cancer and prostate cancer. He is director of the melanoma and sarcoma programs at Montefiore Einstein Center for Cancer Care. In addition, Dr. Packer is medical director of Montefiore's Oncology Care Model (OCM), an alternative payment model sponsored by the Centers for Medicare and Medicaid Services and aimed at improving patient care coordination and appropriateness of care.</p><p>Dr. Packer is the author or co-author of medical textbook chapter and articles in peer-reviewed journals, including <em>Cancer</em>, <em>Clinical Cancer Research</em>, <em>British Medical Journal</em> and <em>Lung Cancer</em>. He is a member of the American Society of Clinical Oncology and the American Society of Hematology.</p>

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Irina Murakhovskaya

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Irina

Last Name

Murakhovskaya

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1235180464

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13953

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<p>Dr. Irina Murakhovskaya is an Assistant Professor of Medicine (Hematology). She completed a medical degree at Albert Einstein College of Medicine and residency and fellowship training at Montefiore Health System. Her clinical interests focus on monoclonal gammopathy, low-grade lymphoma, and hematologic issues in pregnancy.</p>
<p>Dr. Murakhovskaya is currently chairman of the fellowship Clinical Competency Committee and assistant course director for the Albert Einstein of Medicine Hematology Course.&nbsp;</p>

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Haleh Moazen

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Haleh

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Moazen

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1427147750

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3862

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Jincy Mathew

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Jincy

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Mathew

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1639443286

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18330

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5255

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Ioannis Mantzaris

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First Name

Ioannis

Last Name

Mantzaris

NPI

1871865519

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14586

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57027

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Kenneth G. Liu

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Kenneth

Last Name

Liu

NPI

1174840888

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15135

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Kira Gritsman

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First Name

Kira

Last Name

Gritsman

NPI

1174598148

Faculty ID

14128

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part-time

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<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.&nbsp; 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;">&nbsp;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. &nbsp;In hematopoietic cells, there are four isoforms of the catalytic subunit of PI3K, each encoded by a separate gene. &nbsp;Emerging evidence suggests that these isoforms have unique functions in normal and cancer cells, but may substitute for each other in some contexts.&nbsp; 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.&nbsp; 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. &nbsp;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.&nbsp; 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. &nbsp;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&nbsp;</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;">&nbsp;</span><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;">The Gritsman lab&rsquo;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>

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<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.,&nbsp;^&nbsp;Kaur,^&nbsp;I., Shi, Y., Tong, M., Sinclair, T., Hemmati, S., Glushakow-Smith, S.G., Tein,&nbsp;&nbsp;E., Gurska, L., Steidl, U., Dubin, R., Shan, J., Montagna, C., Pradhan, K., Verma, A., and&nbsp;<strong><u>Gritsman, K.</u></strong>, Deletion of PI3-Kinase Promotes Myelodysplasia Through Dysregulation of Autophagy in Hematopoietic Stem Cells,&nbsp;<strong><em>Science Advances</em></strong><em>&nbsp;2023.&nbsp;</em>doi:&nbsp;<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>,&nbsp;</u>PMID:&nbsp;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.,&nbsp;<strong><u>Gritsman, K.</u></strong>&nbsp;&amp; Baker, N.,&nbsp;Haploinsufficiency of the essential gene&nbsp;<em>RpS12</em>&nbsp;causes defects in erythropoiesis and hematopoietic stem cell maintenance,&nbsp;<em>&nbsp;<strong>eLife</strong>&nbsp;</em>2023&nbsp;Jun 5;12:e69322. doi: 10.7554/eLife.69322.&nbsp;PMID:&nbsp;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&nbsp;<strong><u>Gritsman, K.</u></strong>&nbsp;Crizotinib has Preclinical Efficacy in Philadelphia-negative Myeloproliferative Neoplasms,&nbsp;<strong><em>Clinical Cancer Research</em></strong>&nbsp;2022&nbsp;Dec 20:CCR-22-1763. doi: 10.1158/1078-0432.CCR-22-1763. PMID:&nbsp;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&nbsp;<strong><u>Gritsman, K</u></strong>, Signaling Pathways in Leukemic Stem Cells,&nbsp;</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.&nbsp;<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:&nbsp;<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;">;&nbsp;</span>PMID:&nbsp;31338813, PMCID:&nbsp;<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/pmc7249489/&quot; 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&nbsp;<strong><u>Gritsman, K.</u></strong>, PI3 kinase alpha and delta promote hematopoietic stem cell activation,&nbsp;<strong><em>JCI Insight&nbsp;</em></strong>2019&nbsp;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.,&nbsp;<strong><u>Gritsman, K.,&nbsp;</u></strong>and Steidl, U. IL1RAP potentiates multiple oncogenic signaling pathways in AML,&nbsp;<strong><em>Journal of&nbsp;Experimental Medicine</em></strong><em>.&nbsp;</em>2018 May 17. doi: 10.1084/jem.20180147,&nbsp;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&nbsp;<strong><u>Gritsman, K</u>,&nbsp;</strong>Inflammatory Signaling Pathways in Pre-leukemic and Leukemic Stem Cells,&nbsp;<strong><em>Frontiers in Oncology</em></strong><em>&nbsp;</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.,&nbsp;<strong><u>Gritsman, K.,</u></strong>&nbsp;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&nbsp;<strong><em>Cancer Research</em></strong>&nbsp;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.,&nbsp;<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.&nbsp;<strong><em>Nature Communication</em></strong><em>s&nbsp;</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.,&nbsp;<strong><u>Gritsman, K.</u></strong>,&nbsp; 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&nbsp;<strong><em>Nature Medicine</em></strong><em>&nbsp;</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. &nbsp;Hematopoiesis and RAS-driven myeloid leukemia differentially require PI3K isoform p110alpha<strong>.&nbsp;<em>Journal of Clinical Investigation&nbsp;</em></strong>2014;124(4):1794&ndash;1809.&nbsp;http://www.jci.org/articles/view/69927</span></p&gt;
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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&nbsp;<strong><u>Gritsman, K</u></strong>. Akt: A Double-Edged Sword for Hematopoietic Stem Cells.&nbsp;<strong><em>Cell Cycle</em>&nbsp;</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&nbsp;<strong><u>Gritsman, K</u>.</strong>&nbsp;Constitutively Active AKT Depletes Hematopoietic Stem Cells and Induces Leukemia in Mice.&nbsp;<strong><em>Blood&nbsp;</em></strong>2010; 115(7): 140615&nbsp;http://www.bloodjournal.org/content/115/7/1406</span></p&gt;
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EMR ID

73180

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Swati Goel

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First Name

Swati

Last Name

Goel

NPI

1053632869

Faculty ID

13662

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<p>Dr. Swati&nbsp;Goel is an Assistant Professor of Medicine (Hematology). &nbsp;She completed medical school education&nbsp;at the All India Institute of Medical Sciences and finished postgraduate hematology-oncology&nbsp;training at NYU Langone Medical Center.</p>
<p>Dr. Goel sees patients with blood disorders and blood-related cancers.&nbsp;She&nbsp;specializes in the field&nbsp;of myeloproliferative disorders like myelofibrosis, polycythemia vera, and essential thrombocytosis. She is the leader of Myeloproliferative Disorder Clinic at Montefiore Einstein.</p>

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Myeloproliferative neoplasms, and the conditions she treats include myelofibrosis, polycythemia vera, essential thrombocythemia, mastocytosis, eosinophilia, anemia and pancytopenia.

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Myeloproliferative neoplasms

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EMR ID

4908

Biography

<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&rsquo;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>

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Howard Geyer

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First Name

Howard

Last Name

Geyer

NPI

1235298688

Faculty ID

10183

CMO Specialties

Clinical Terms

Employment Status

Full Time

Patient Type

Adult

Department

Gender

Male

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Phone

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Education and Trainings

Professional Interests

<p>Dr. Howard Geyer is Director, Division of Movement Disorders, Montefiore, and Assistant Professor, Neurology, Albert Einstein College of Medicine.&nbsp;He received his MD and PhD degrees from the University of Pennsylvania.&nbsp;He was chief resident in Neurology at Montefiore, where he also completed a fellowship in Clinical Neurophysiology.&nbsp;He completed an additional fellowship in Movement Disorders at Beth Israel Medical Center.&nbsp;Dr. Geyer regularly lectures and contributes to book chapters and journal articles on a variety of neurologic topics.</p>

Research Profile

Clinical Profile

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Professional Title

Elsevier Profile

EMR ID

4312

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