Della F. Makower

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Della

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Makower

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1578559910

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6729

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<p>My research is focused on breast cancer management, and on care delivery and support for breast cancer patients.&nbsp;</p>

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3965

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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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Adam S. Levy

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First Name

Adam

Last Name

Levy

NPI

1710065974

Faculty ID

9837

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Per Diem

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Pediatric

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Male

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<p>Dr. Levy, Director of Pediatric Neuro-Oncology at The Children&rsquo;s Hospital at Montefiore, was the principal investigator for the Children&rsquo;s Oncology Group, the nation's largest consortium of childhood cancer researchers, and currently leads an international clinical trial for children with recurrent brain tumors. Dr. Levy&rsquo;s clinical interests focus on brain tumors, particularly new drugs and treatment plans for children with brain tumors.</p>
<p>As Associate Professor of Clinical Pediatrics at Albert Einstein College of Medicine, Dr. Levy also has a strong interest in medical education. He is director of the pediatric hematology/oncology fellowship training program, and he is chair of the Committee on Graduate Medical Education.</p>
<p>After graduating from Cornell University, Dr. Levy received his medical degree from NYU School of Medicine. He was a Chief Resident in Pediatrics at Mount Sinai Medical Center, where he received the Department of Pediatrics Resident Clinician-Teacher Award. He then completed his fellowship and was Chief Fellow in Pediatric Hematology and Oncology at Memorial Sloan-Kettering Cancer Center and New York Hospital/Weill Cornell Medical Center, where he received the Charles Trobman Memorial Award.&nbsp; He was nominated Attending Physician of the Year in Pediatrics at NYU Medical Center before joining Montefiore and Einstein. In 2007 he received a Children&rsquo;s Tumor Foundation Humanitarian Award for his care of children with tumors associated with neurofibromatosis, and in 2011 he was elected to the Society for Pediatric Research.&nbsp;</p>
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<p>Brain and spinal cord tumors; pediatric solid tumors; neurofibromatosis</p>

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<p>Dr. Levy practices general pediatric hematology-oncology with a focus on tumors of the brain and spine. Dr. Levy&rsquo;s current research interests concern the use of new drugs and treatment plans for children with cancer.</p>

Elsevier Profile

EMR ID

4667

Biography

<p>Adam Levy, MD, is a Clinical Professor who works per diem at Montefiore Einstein in the trainee&rsquo;s clinic. He specializes in general pediatric hematology and oncology, with a focus on tumors of the brain and spine, solid tumors and tumors associated with neurofibromatosis.</p><p>After receiving his Bachelor of Science at Cornell University, Dr. Levy earned his Doctor of Medicine at New York University School of Medicine. Following this, he completed training in pediatrics at Mount Sinai Medical Center in New York and became Chief Resident. Dr. Levy then completed a pediatric hematology/oncology fellowship at Memorial Sloan-Kettering and New York Hospital/Weill Cornell Medical Center, where he served as Chief Fellow.</p><p>Dr. Levy&rsquo;s early research training in a transitional science laboratory focused on mechanisms and pathways explaining tumor cell chemotherapy resistance. He was the principal investigator for the Children&rsquo;s Oncology Group, the nation's largest consortium of childhood cancer researchers, and currently leads an international clinical trial for children with recurrent brain tumors. As a clinical investigator, his current research focuses on using new drugs and treatment plans for pediatric cancer patients. He has studied and published ways to improve clinical care of patients, mentorship in pediatric oncology, communication skills training and burnout amongst clinicians. He has been an invited presenter on these topics nationally.</p><p>Dr. Levy is a member of the Society for Pediatric Research, and his efforts have been recognized numerous times as a New York Magazine Top Doctor. He has also won many awards, including the Children&rsquo;s Tumor Foundation Humanitarian Award, The Davidoff Society Education Award and the Charles Trobman Memorial Award.</p>

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Noah Kornblum

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Noah

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Kornblum

NPI

1053461517

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13153

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Non-Hodgkin Lymphoma&nbsp;<br /><br />

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4258

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Ross I. Kaye

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First Name

Ross

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Kaye

NPI

1568737831

Faculty ID

18024

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78694

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Rasim A. Gucalp

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First Name

Rasim

Last Name

Gucalp

NPI

1295815785

Faculty ID

4777

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<p>Dr. Rasim Gucalp&rsquo;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.&nbsp;</p>

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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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Female

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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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D. Yitzchak Goldstein

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First Name

D. Yitzchak

Last Name

Goldstein

NPI

1295014991

Faculty ID

15128

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<p>Dr. Goldstein completed his medical school training at Einstein and went on to complete his residency and chief residency in anatomic and clinical pathology at Montefiore. With a passion for advanced molecular diagnostics he then went on to complete a molecular genetic pathology fellowship and Mount Sinai hospital.</p>
<p>Dr. Goldstein&rsquo;s interests include several areas of clinical laboratory medicine and laboratory optimization with particular interests in molecular diagnostics and data alanysis. Dr. Goldstein has received accolades for his teaching including the Leo M. Davidoff award for teaching of medical students at Einstein as well as the Montefiore Pathology Department resident teaching award. Dr. Goldstein currently serves as Associate Director of Molecular Infectious Disease Testing and is Co-Director of the Molecular Genetic laboratories at Montefiore.</p>

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Selected Publications

<p>Jacob, J., <strong>Goldstein, DY.</strong>, &amp; Gil, M. R. (2019). Molecular Testing in Coagulation. In&nbsp;<em>Transfusion Medicine and Hemostasis</em>&nbsp;(pp. 945-953). Elsevier.</p>
<p>Marks, E., Wang, Y., Shi, Y., Susa, J., Jacobson, M., &amp; <strong>Goldstein, D. Y</strong>. (2018). Specific TCR gene rearrangements in mycosis fungoides: does advanced clinical stage show a preference?.&nbsp;<em>Journal of clinical pathology</em>,&nbsp;<em>71</em>(12), 1072-1077</p>
<p>Patel, S. R., Madan, S., Saeed, O., <strong>Goldstein, D.Y.</strong>, Shin, J. J., Nucci, C., ... &amp; Vukelic, S. (2018). Cardiac transplantation from non-viremic hepatitis C donors.&nbsp;<em>The Journal of Heart and Lung Transplantation</em>,&nbsp;<em>37</em>(10), 1254-1260.</p>
<p>Kim, T., Khader, S. N., &amp; <strong>Goldstein, D. Y.</strong> (2018). Educational Case: Cervical Neoplasia: HPV and Its Link to Cancer.&nbsp;<em>Academic Pathology</em>,&nbsp;<em>5</em>, 2374289518770651.</p>
<p>Castellucci, E., He, T., <strong>Goldstein, D. Y.</strong>, Halmos, B., &amp; Chuy, J. (2017). DNA polymerase ɛ deficiency leading to an ultramutator phenotype: a novel clinically relevant entity.&nbsp;<em>The oncologist</em>,&nbsp;<em>22</em>(5), 497-502.</p>
<p><strong>Goldstein, D. Y.,</strong> &amp; Prystowsky, M. (2017). Educational Case: Autosomal Recessive Inheritance: Cystic Fibrosis.&nbsp;<em>Academic pathology</em>,&nbsp;<em>4</em>, 2374289517691769.</p>

EMR ID

54210

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Mendel Goldfinger

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First Name

Mendel

Last Name

Goldfinger

NPI

1801174792

Faculty ID

16256

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Full Time

Patient Type

Adult

Department

Gender

Male

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Professional Interests

<p>Dr. William Osler famously said, &ldquo;The good physician treats the disease; the great physician treats the patient who has the disease.&rdquo; 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&rsquo;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&rsquo;s immune system to fight cancer and research how to enhance their tumor&rsquo;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&rsquo;s tumor. Every patient&rsquo;s regimen is tailored by identifying and targeting the tumor&rsquo;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&mdash;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>

Research Profile

Clinical Profile

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Off

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Elsevier Profile

EMR ID

54204

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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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Full Time

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Adult

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Female

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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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Clinical Focus

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

Research Focus

Myeloproliferative neoplasms

Elsevier Profile

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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