Irina Murakhovskaya

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Irina

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Murakhovskaya

NPI

1235180464

Faculty ID

13953

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Female

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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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4308

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Kerry A. Morrone

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First Name

Kerry

Last Name

Morrone

NPI

1265734297

Faculty ID

12909

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Pediatric

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Female

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<p>Anemia, hospitalist medicine, general pediatrics</p>

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Dr. Morrone focuses on classical hematology, particularly sickle cell disease and hemoglobinopathies, platelet disorders, thrombosis, and bone marrow failure syndromes.

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Dr. Morrone is committed to improving quality of care and health care utilization in chronic illness, particularly sickle cell disease, and thalassemia through her research

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EMR ID

4700

Biography

<p>Kerry Morrone, MD, is an Assistant Professor of Pediatrics at the Albert Einstein College of Medicine, the Director of the Sickle Cell Program and the Director of the Pediatric Hematology Oncology Fellowship Program at Montefiore. Dr. Morrone focuses on classical hematology, particularly sickle cell disease and hemoglobinopathies, platelet disorders, thrombosis, and bone marrow failure syndromes.</p><p>Dr. Morrone graduated from New York University, earning her Bachelor of Arts in Biology in 2003. She then attended the Albert Einstein College of Medicine, where she received her Doctor of Medicine in 2007 and was inducted into the Alpha Omega Alpha Honor Medical Society. Dr. Morrone completed her pediatric residency, chief residency, and pediatric hematology oncology fellowship all at the Albert Einstein College of Medicine. She has also been recognized for her teaching efforts many times and won the Leo M. Davidoff Society &ndash; Albert Einstein College of Medicine Teaching Award in 2010 and 2015.</p><p>Dr. Morrone is committed to improving quality of care and health care utilization in chronic illness, particularly sickle cell disease, and thalassemia through her research. Other current research interests include pulmonary complications of sickle cell disease particularly asthma and acute chest syndrome, in addition to infectious complications and thrombotic complications of sickle cell disease.</p>

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Katharine A. McNeill

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First Name

Katharine

Last Name

McNeill

NPI

1598995730

Faculty ID

15494

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1542

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Allison M. Martin

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Allison

Last Name

Martin

NPI

1710200654

Faculty ID

15926

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Full Time

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Pediatric

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Female

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EMR ID

102070

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<p>Allison M. Martin, MD, is an attending physician at the Children&rsquo;s Hospital at Montefiore Einstein and Assistant Professor, Pediatrics, Microbiology and Immunology at our Albert Einstein College of Medicine. Dr. Martin&rsquo;s clinical focus centers on pediatric brain and spinal cord tumors.</p><p>After receiving her Bachelor of Arts in biology from Bryn Mawr College in 2001, Dr. Martin earned her Doctor of Medicine at Jefferson Medical College in 2007. She completed her pediatrics residency at the University of Pittsburgh in 2010, followed by a pediatric hematology/oncology fellowship at the Johns Hopkins University School of Medicine and the National Institutes of Health in 2013. Following this, Dr. Martin completed an additional fellowship in pediatric neuro-oncology at the Johns Hopkins University School of Medicine in 2014.</p><p>Dr. Martin&rsquo;s research focuses on high-risk group 3 and refractory medulloblastoma. Her research program focuses on uncovering new ways to harness the immune system to treat this disease. Her work has been shared through numerous peer-reviewed publications, abstracts, case reports and invited talks and panels. She has also been principal investigator and co-investigator on several funded research projects and is a reviewer for <em>Cancers</em>.</p><p>Dr. Martin is board certified in Pediatrics and Pediatric Hematology-Oncology. She is a member of the Children&rsquo;s Oncology Group (COG), the Cancer Therapy Evaluation Program (CTEP) and the Society of Immunotherapy and Cancer (SITC). In 2021, Dr. Martin received the Pediatric Hematology/Oncology Fellows Teaching Award from the Children&rsquo;s Hospital at Montefiore Einstein. She was named a &ldquo;Top Doctor&rdquo; by Castle Connolly in 2024.</p>

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Ioannis Mantzaris

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First Name

Ioannis

Last Name

Mantzaris

NPI

1871865519

Faculty ID

14586

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Full Time

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Male

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EMR ID

57027

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Della F. Makower

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First Name

Della

Last Name

Makower

NPI

1578559910

Faculty ID

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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First Name

Kenneth

Last Name

Liu

NPI

1174840888

Faculty ID

15135

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57009

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Noah Kornblum

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First Name

Noah

Last Name

Kornblum

NPI

1053461517

Faculty ID

13153

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

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4258

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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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<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>
<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><em><span style="font-size: 11pt; font-family: Arial, sans-serif;">&nbsp;</span></em></p>
<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

Is Open Scheduling

Off