Irina Murakhovskaya

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Irina

Last Name

Murakhovskaya

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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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Lisa Morrow

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Lisa

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Morrow

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1174849640

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15916

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Nurse Practitioner

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6363

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Tania V. Marin Saquicela

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Tania

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Marin Saquicela

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1316471758

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16725

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Female

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Primary Care

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2577

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Ioannis Mantzaris

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Ioannis

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Mantzaris

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1871865519

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14586

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Rishi Malhotra

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Rishi

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Malhotra

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1154509933

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14085

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<span style="caret-color:#000000;font-family:Calibri, Arial, Helvetica, sans-serif;font-size:16px;text-size-adjust:auto;background-color:#ffffff;">Subarachnoid hemorrhage, Intracerebral Hemorrhage, Ischemic Stroke, Status Epilepticus, Neuromuscular Respiratory Failure, CNS Infections</span>

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<span style="caret-color:#000000;font-family:Calibri, Arial, Helvetica, sans-serif;font-size:16px;text-size-adjust:auto;background-color:#ffffff;">Intracerebral Hemorrhage</span>

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5784

Biography

<p>Rishi Malhotra, MD, is Director of Neurocritical Care, Director of the Neuroscience ICU and Director of the Neurocritical Care Fellowship, as well as Associate Professor of Neurology, Medicine and Neurological Surgery at Montefiore Einstein. Dr. Malhotra&rsquo;s clinical focus includes the critical care management of subarachnoid hemorrhage, intracerebral hemorrhage, traumatic brain injury, acute spinal cord injury, ischemic stroke, status epilepticus, brain tumors, neuromuscular respiratory failure and central nervous system infections.</p><p>A graduate of the combined BA/MD program at Brooklyn College, Dr. Malhotra completed his Doctor of Medicine with State University of New York - Downstate Medical Center in 2004. After completing his internal medicine internship at St. Luke&rsquo;s-Roosevelt Hospital in 2005, Dr. Malhotra completed his three-year neurology residency at Columbia University Medical Center in 2008. He then pursued a neurocritical care fellowship at Columbia University Medical Center and Weill Cornell Medical Center, which he completed in 2010.</p><p>Dr. Malhotra&rsquo;s scholarly interests include intracerebral hemorrhage, hypoxic-ischemic brain injury and status epilepticus. He has shared his work through peer-reviewed journals, books, abstracts and poster presentations.</p><p>Dr. Malhotra is board certified in Neurology and Neurocritical Care. He is a member of the Neurocritical Care Society.</p>

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Kenneth G. Liu

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Kenneth

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Liu

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1174840888

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15135

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Mahsa Kanzali

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Mahsa

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Kanzali

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1295122661

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18306

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Nicole A. Hayde

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Nicole

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Hayde

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1417196726

Faculty ID

11790

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Pediatric

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Female

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On

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EMR ID

54328

Biography

<p>Nicole Hayde, MD, MS, is a pediatric nephrologist at Children&rsquo;s Hospital at Montefiore Einstein (CHAM), Medical Director, Pediatric Kidney Transplant Program, Associate Director, Pediatric Nephrology Fellowship Program and Associate Professor, Pediatrics at Montefiore-Einstein. Dr. Hayde&rsquo;s clinical focus is pediatric renal transplantation, with a particular interest in the role of antibodies in allograft injury.</p><p>After earning her Doctor of Medicine from the University of the West Indies, Mona, Jamaica in 2003, Dr. Hayde completed her residency and chief residency in pediatrics at the University of Miami in 2009. She went on to complete her fellowship in pediatric nephrology at CHAM in 2012. During her fellowship, she was also enrolled in the clinical research training program at Einstein, earning her Master of Science in clinical research methods in 2012.</p><p>Dr. Hayde&rsquo;s research focus is on the role of donor-specific antibodies in pediatric kidney transplantation and methods to decrease antibody mediated injury. Her findings have been published in several peer-reviewed journals, and have been shared through book chapters, posters and presentations. She is on the editorial board of Frontiers in Pediatrics and is a peer reviewer for several journals including Transplantation, Pediatric Transplantation and Human Immunology. She also serves as a research mentor for fellows interested in kidney transplant research.</p><p>Dr. Hayde is board certified in pediatrics and pediatric nephrology. She has several national roles including the associate councilor of region 9 of United Network of Organ Sharing (UNOS) and the executive committee of the pediatric community of practice of the American Society of Transplantation. She is also a member of several professional organizations including the ASPN and the American Society of Histocompatibility and Immunogenetics.</p>

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Kira Gritsman

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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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Selected Publications

<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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Valentyna Goloborodko

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Valentyna

Last Name

Goloborodko

NPI

1194010728

Faculty ID

13925

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Female

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Elsevier Profile

EMR ID

5492

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