Allison M. Martin
<p>Allison M. Martin, MD, is an attending physician at the Children’s Hospital at Montefiore Einstein and Assistant Professor, Pediatrics, Microbiology and Immunology at our Albert Einstein College of Medicine. Dr. Martin’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’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’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’s Hospital at Montefiore Einstein. She was named a “Top Doctor” by Castle Connolly in 2024.</p>
Ioannis Mantzaris
Della F. Makower
<p>My research is focused on breast cancer management, and on care delivery and support for breast cancer patients. </p>
Kenneth G. Liu
Adam S. Levy
<p>Dr. Levy, Director of Pediatric Neuro-Oncology at The Children’s Hospital at Montefiore, was the principal investigator for the Children’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’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. 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’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. </p>
<p> </p>
<p>Brain and spinal cord tumors; pediatric solid tumors; neurofibromatosis</p>
<p>Dr. Levy practices general pediatric hematology-oncology with a focus on tumors of the brain and spine. Dr. Levy’s current research interests concern the use of new drugs and treatment plans for children with cancer.</p>
<p>Adam Levy, MD, is a Clinical Professor who works per diem at Montefiore Einstein in the trainee’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’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’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’s Tumor Foundation Humanitarian Award, The Davidoff Society Education Award and the Charles Trobman Memorial Award.</p>
Dominique M. Jan
<span style="color:#4d4d4d;font-family:Arial, Helvetica, source-code-pro, Menlo, Monaco, Consolas, 'Courier New', monospace;font-size:16px;background-color:#ffffff;">Pediatric Surgery</span><quillbot-extension-portal></quillbot-extension-portal>
Dr. Jan's research focus is in the areas of pediatric transplantation of the small bowel, liver and kidney.<quillbot-extension-portal></quillbot-extension-portal>
<p>Dominique M. Jan, MD received his medical degree from the Université Pierre-et-Marie-Curie in Paris.</p><p>He completed his internship and residency in general surgery with special training in pediatric surgery, urology, surgery of the digestive tract and vascular surgery at the Assistance publique – Hôpitaux de Paris. He fulfilled fellowship training in pediatric surgery at the Hôpital Necker – Enfants Malades in Paris and is board certified by the French Boards for General Surgery and Pediatric Surgery.</p><p>Dr. Jan is a member of numerous leading international professional societies and has published and presented more than 100 articles in the areas of pediatric transplantation of the small bowel, liver and kidney.</p><p>Prior to assuming his current role of Chief, Division of Pediatric Surgery, and Director, Pediatric Transplantation Surgery, Professor of Surgery, Albert Einstein College of Medicine, he served as attending surgeon in the Department of Surgery at the Columbia University Medical Center, attending physician at the Hôpital Necker – Enfants Malades and as deputy chair of Pediatric Surgery at the Hôpital Saint Camille in Paris.</p>
Rasim A. Gucalp
<p>Dr. Rasim Gucalp’s research interests include novel therapies in lung cancer as well as supportive care in cancer patients. He is actively involved in the multidisciplinary care of patients with lung cancer and central nervous system tumors. He is a member of several Montefiore Medical Center/Albert Einstein College of Medicine committees including the institutional tumor board, faculty senate, Pharmacy and Therapeutic Committee, and COGME.</p>
<p>A native of Turkey, Dr. Gucalp received his medical degree at Hacettepe University School of Medicine in Ankara, Turkey. After completing his medical residency at Downstate Medical Center in Brooklyn, he came to Montefiore Medical Center to complete his oncology fellowship. He is the director of the Hematology/Oncology Fellowship Program at Montefiore, and serves as a professor of Clinical Medicine at Albert Einstein College of Medicine. </p>
Kira Gritsman
<p><strong>The Roles of Signaling Pathways in Adult Blood Development and Leukemia</strong></p>
<p><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;">The Gritsman lab studies the signal transduction pathways that affect the early fate decisions of adult hematopoietic stem cells (HSCs) as they progress from an undifferentiated multipotent state to the generation of differentiated blood cells. When these early fate decisions go awry, this can lead to the formation of leukemia-initiating cells. We are interested in</span><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;"> how signaling pathways affect the self-renewal and differentiation of HSCs and malignant or pre-malignant stem cells in myeloid malignancies, such as acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and myeloproliferative neoplasms (MPN).</span></p>
<p><strong>Roles of the PI3 kinase isoforms in adult blood development</strong></p>
<p>PI3 kinase (PI3K) is a lipid kinase that is important for the regulation of metabolism, the cell cycle, apoptosis, and protein synthesis. In hematopoietic cells, there are four isoforms of the catalytic subunit of PI3K, each encoded by a separate gene. Emerging evidence suggests that these isoforms have unique functions in normal and cancer cells, but may substitute for each other in some contexts. We have generated a series of mouse knockout models that allow us to study the roles of each of these isoforms individually in adult hematopoiesis. For example, we have found that the p110alpha isoform is most important for red cell development, but is not required in normal blood stem cells. We have now also generated compound knockout mice to determine the redundant roles of the PI3K isoforms in blood development. We recently reported that PI3K isoforms play important redundant roles during the hematopoietic stress response, such as after chemotherapy. However, deletion of all 3 Class IA PI3K isoforms leads to a phenotype with impaired HSC differentiation, resembling myelodysplastic syndrome (MDS). We are studying how deletion of PI3K will impact normal HSC function, including self-renewal, proliferation, and differentiation along different blood lineages by affecting processes such as autophagy and epigenetic regulation in HSCs.</p>
<p><strong>Roles of the PI3 kinase isoforms in leukemia</strong></p>
<p>Acute myeloid leukemia (AML) is a genetically diverse disease, but activation of the PI3K pathway has been reported in up to 80% of cases. A subset of AML cell lines and AML patient samples respond to PI3K pathway inhibitors, but it is unclear how patients should be selected for potential response to these inhibitors. We found that RAS-mutated myeloid leukemias are particularly dependent on the p110alpha isoform of PI3K, and that pharmacologic inhibition of p110alpha can be used to treat both RAS-mutated cell lines and RAS-mutated leukemia in mice. Furthermore, we use cell lines, patient samples, and mouse models of leukemia to investigate the mechanisms of resistance to PI3K inhibition, with the goal of identifying new drug targets and designing new combination treatments for leukemia that incorporate PI3K inhibitors.</p>
<p><strong>RON Kinase in Myeloproliferative Neoplasms</strong></p>
<p>The myeloproliferative neoplasms (MPNs) are a group of diseases that are caused by kinase mutations in HSCs, which lead to uncontrolled proliferation of myeloid cells. The Philadelphia chromosome-negative MPNs are characterized by mutations in the JAK/STAT signaling pathway, and respond to JAK inhibitors, but resistance often develops. We recently discovered that the receptor Tyrosine kinase RON can physically interact with JAK2 in MPN cells, leading to potentiation of JAK/STAT signaling in resistant cells. Furthermore, we found that pharmacologic or genetic inactivation of RON can inhibit proliferation of MPN cells and re-sensitize resistant cells to JAK inhibitors.</p>
<p class="MsoNormal" style="margin: 0in 0in 0.0001pt; font-size: medium; font-family: 'Times New Roman', serif;"><strong><span style="font-size: 10.5pt; font-family: Verdana, sans-serif; color: #201f1e;">Member of the Cancer Dormancy and Tumor Microenvironment Institute </span></strong></p>
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<p class="MsoNormal" style="margin: 0in 0in 0.0001pt; font-size: medium; font-family: 'Times New Roman', serif;"><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;"> </span><span style="font-size: 10.5pt; font-family: Verdana, sans-serif;">The Gritsman lab’s research interests include the contributions of signaling pathways to leukemic and pre-leukemic stem cell dormancy in minimal residual disease, which includes mechanisms of immune evasion. Furthermore, the Gritsman lab is interested in the roles of inflammatory signaling pathways and of the local microenvironment in bone marrow fibrosis, and in the evolution of myeloid neoplasms from the pre-malignant to malignant state. Our major goals are to identify opportunities for therapeutic targeting to prevent the transition from the pre-leukemic state to leukemia, or to eliminate minimal residual disease to prevent relapse.</span></p>
<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><a name="_GoBack"></a><span style="font-size: 11pt; font-family: Arial, sans-serif;">Ames, K., <sup> </sup>Kaur,<sup> </sup>I., Shi, Y., Tong, M., Sinclair, T., Hemmati, S., Glushakow-Smith, S.G., Tein, E., Gurska, L., Steidl, U., Dubin, R., Shan, J., Montagna, C., Pradhan, K., Verma, A., and <strong><u>Gritsman, K.</u></strong>, Deletion of PI3-Kinase Promotes Myelodysplasia Through Dysregulation of Autophagy in Hematopoietic Stem Cells, <strong><em>Science Advances</em></strong><em> 2023. </em>doi: <a href="https://nam04.safelinks.protection.outlook.com/?url=https%3A%2F%2Fdoi.o…; target="_blank" rel="noopener"><span style="color: black; text-decoration: none;">10.1126/sciadv.ade8222</span></a><u>, </u>PMID: 36812307</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Folgado Marco, V., Ames, K., Chuen, J., <strong><u>Gritsman, K.</u></strong> & Baker, N., Haploinsufficiency of the essential gene <em>RpS12</em> causes defects in erythropoiesis and hematopoietic stem cell maintenance, <em> <strong>eLife</strong> </em>2023 Jun 5;12:e69322. doi: 10.7554/eLife.69322. PMID: 37272618</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Gurska, L.M., Okabe, R., Schurer, A., Tong, M.M., Soto, M., Choi, D., Ames, K., Glushakow-Smith, S., Montoya, A., Tein, E., Miles, L.A., Cheng, H., Hankey-Giblin, P., Levine, R.L., Goel, S., Halmos, B., and <strong><u>Gritsman, K.</u></strong> Crizotinib has Preclinical Efficacy in Philadelphia-negative Myeloproliferative Neoplasms, <strong><em>Clinical Cancer Research</em></strong> 2022 Dec 20:CCR-22-1763. doi: 10.1158/1078-0432.CCR-22-1763. PMID: 36537918</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Gurska, L., Ames, K., and <strong><u>Gritsman, K</u></strong>, Signaling Pathways in Leukemic Stem Cells, </span><span style="font-size: 11pt; font-family: Arial, sans-serif; color: #333333; letter-spacing: 0.2pt; background-color: #fcfcfc;">In: Zhang H., Li S. (eds) Leukemia Stem Cells in Hematologic Malignancies. <strong>Advances in Experimental Medicine and Biology</strong>, vol 1143. Springer, Singapore</span><span style="font-size: 11pt; font-family: Arial, sans-serif;">, July 24, 2019, doi: <a href="https://doi.org/10.1007/978-981-13-7342-8_1"><span style="color: black; letter-spacing: 0.2pt; background-color: #fcfcfc; text-decoration: none;">https://doi.org/10.1007/978-981-13-7342-8_1</span></a><span style="letter-spacing: 0.2pt; background-color: #fcfcfc;">; </span>PMID: 31338813, PMCID: <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/pmc7249489/" target="_blank" rel="noopener"><span style="color: black; text-decoration: none;">PMC7249489</span></a></span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Hemmati, S., Sinclair, T., Tong, M., Bartholdy, B., Okabe, R.O., Ames, K., Ostrodka, L., Haque, T., Kaur, I., Mills, T. S., Agarwal, A., Pietras, E.M., Zhao, J.J., Roberts, T.M., and <strong><u>Gritsman, K.</u></strong>, PI3 kinase alpha and delta promote hematopoietic stem cell activation, <strong><em>JCI Insight </em></strong>2019 doi.org/10.1172/jci.insight.125832</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Mitchell, K., Barreyro, L., Todorova, T., Taylor, S., Antony-Debre, I., Narayanagari, S., Carvajal, L., Leite, J., Piperdi, Z., Pendurti, G., Mantzaris, I., Paietta, E., Verma, A., <strong><u>Gritsman, K., </u></strong>and Steidl, U. IL1RAP potentiates multiple oncogenic signaling pathways in AML, <strong><em>Journal of Experimental Medicine</em></strong><em>. </em>2018 May 17. doi: 10.1084/jem.20180147, PMID: 29773641</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Hemmati, S., Haque, T., and <strong><u>Gritsman, K</u>, </strong>Inflammatory Signaling Pathways in Pre-leukemic and Leukemic Stem Cells, <strong><em>Frontiers in Oncology</em></strong><em> </em>2017 Nov 13;7:265. doi: 10.3389/fonc.2017.00265</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Bhagat, T.D., Chen, S., Bartenstein, M., Barlowe, A.T., Von Ahrens, D., Choudhary, G.S., Tivnan, P., Amin, E., Marcondes, M., Sanders, M.A., Hoogenboezem, R.M., Kambhampati, S., Ramanchandra, N., Mantzaris, I., Sukrithan, V., Laurence, R., Lopez, R. Bhagat, P., Giricz, O., Sohal, D., Wickrema, A., Yeung, C., <strong><u>Gritsman, K.,</u></strong> Aplan, P., Hochedlinger, K., Yu, Y., Pradhan, K., Zhang, J., Greally, J.M., Mukherjee, S., Pellagatti, A., Boultwood, J., Will, B., Steidl, U., Raaijmakers, M.H.G.P., Deeg, H.J., Kharas, M.G. and Verma, A. Epigenetically Aberrant Stroma in MDS Propagates Disease Via Wnt/b-Catenin Activation, 2017 <strong><em>Cancer Research</em></strong> 2017 Jul 6. pii: canres.0282.2017. doi: 10.1158/0008-5472</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Yuzugullu, H., Baitsch, L., Von, T., Steiner, A., Tong, H., Ni, J., Clayton, L., Bronson, R., Roberts, T., <strong><u>Gritsman, K</u></strong><u>.</u>, and Zhao, J.J. A p110b-Rac signaling loop mediates Pten-loss-induced perturbation of hematopoiesis and leukemogenesis. <strong><em>Nature Communication</em></strong><em>s </em>October 7,2015, doi:10.1038/NCOMMS9501</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Yoda, A., Adelmant, G., Tamburini, J., Chapuy, B., Shindoh, N., Yoda, Y., Weigert, O., Kopp, N., Wu, S-C., Kim, S., Liu, H., Tivey, T., Christie, A.L., <strong><u>Gritsman, K.</u></strong>, Gotlib, J., Deininger, M., Turley, S., Tyner, J., Marto, J., Weinstock, D.M., and Lane, A.A. Mutations in G-protein beta subunits promote transformation and kinase inhibitor resistance <strong><em>Nature Medicine</em></strong><em> </em>2015 (1):71-5.</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><strong><u><span style="font-size: 11pt; font-family: Arial, sans-serif;">Gritsman, K</span></u></strong><strong><span style="font-size: 11pt; font-family: Arial, sans-serif;">.</span></strong><span style="font-size: 11pt; font-family: Arial, sans-serif;">, Yuzugullu, H., Von, T., Yan, H., Clayton, L., Fritsch, C., Maira, S.-M., Hollingworth, G., Choi, C., Khandan, T., Paktinat, M., Okabe, R.O., Roberts, T.M., and Zhao, J.J. Hematopoiesis and RAS-driven myeloid leukemia differentially require PI3K isoform p110alpha<strong>. <em>Journal of Clinical Investigation </em></strong>2014;124(4):1794–1809. http://www.jci.org/articles/view/69927</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Kharas, M.G. and <strong><u>Gritsman, K</u></strong>. Akt: A Double-Edged Sword for Hematopoietic Stem Cells. <strong><em>Cell Cycle</em> </strong>2010; Vol 9; Issue 7</span></p>
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<p class="MsoNormal" style="margin: 0in; font-size: medium; font-family: Calibri, sans-serif;"><span style="font-size: 11pt; font-family: Arial, sans-serif;">Kharas, M.G., Okabe, R., Ganis, J.J., Gozo,M., Khandan,T., Paktinat, M., Gilliland, D.G., and <strong><u>Gritsman, K</u>.</strong> Constitutively Active AKT Depletes Hematopoietic Stem Cells and Induces Leukemia in Mice. <strong><em>Blood </em></strong>2010; 115(7): 140615 http://www.bloodjournal.org/content/115/7/1406</span></p>
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Lisa M. Figueiredo-Gennarini
Dr. Gennarini’s clinical practice focuses on treatment of children with leukemia and lymphoma as well as various vascular anomalies. She is a member of the Dana Farber Cancer Institute Acute Lymphoblastic Leukemia Consortium and the CHAM Principal Investigator for Children’s Oncology Group trials. Dr. Gennarini also leads the CHAM Vascular Malformations Program
<p>Lisa Gennarini, MD, has been an Assistant Professor of Pediatrics in the Division of Pediatric Hematology/Oncology and Blood & Marrow Cell Transplantation at Children's Hospital at Montefiore (CHAM) since 2014. Her clinical focus is on treatment of children with leukemia and lymphoma as well as various vascular anomalies. She is also the CHAM Principal Investigator for Children?s Oncology Group trials, and also leads the CHAM Vascular Malformations Program. </p><p>Dr. Gennarini graduated from Siena College in 2004, earning her Bachelor of Science in Biology. In 2008, she received her Doctor of Medicine at State University of New York, Upstate Medical University in Syracuse. She began a residency in Pediatrics at Jefferson Medical College/A.I. duPont Hospital for Children, followed by a fellowship in Pediatric Hematology/Oncology at Children?s Hospital at Montefiore. </p><p>Dr. Gennarini's work on pediatrics, topics ranging from sickle cell disease to implementing communications skills training courses in pediatric hematology/oncology, has been published in various journals and books, and presented nationally. </p><p>Dr. Gennarini is board certified by the American Board of Pediatrics in Pediatric Hematology/Oncology and General Pediatrics. </p>