Director, Hematologic Malignancies and Co-Leader, Experimental Therapeutics Program, University of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center
(410) 328-8085 lab
Education and Training
Education and Training:
-B.A. Harvard University, magna cum laude
-M.D. Johns Hopkins University School of Medicine
-Resident, Internal Medicine, Vanderbilt University
-Fellowship, Hematology Vanderbilt University
-National Research Service trainee, Vanderbilt University
Maria R. Baer, M.D. joined the University of Maryland Marlene and Stewart Greenebaum Cancer Center as Director of Hematologic Malignancies in April, 2007, and also became Co-Leader of the University of Maryland Marlene and Stewart Greenebaum Cancer Center Experimental Therapeutics Program in July 2014. She is Professor of Medicine and Professor of Molecular Medicine, University of Maryland School of Medicine. She previously served as Chief of the Leukemia Section of Roswell Park Cancer Institute and was Professor of Medicine and Associate Professor of Molecular Pharmacology and Cancer Therapeutics at the University at Buffalo School of Medicine and Biomedical Sciences. She has a long track record of single-institution, multi-institution and cooperative group clinical and translational research in acute leukemia and myelodysplastic and myeloproliferative neoplasms. In the cooperative group setting, she served as principal investigator of a phase 3 clinical trial of multidrug resistance modulation and immune modulation in previously untreated older acute myeloid leukemia patients (Cancer and Leukemia Group B [CALGB] 9720) and of immunophenotyping (CALGB 8361) and drug resistance (CALGB 9760) correlative science protocols. She is a longstanding member of the CALGB/Alliance for Clinical Trials in Oncology Leukemia and Leukemia Correlative Sciences Core Committees and a member of the Stand Up to Cancer Epigenetics Dream Team. Her laboratory works on mechanisms of drug resistance in acute myeloid leukemia and approaches to overcoming drug resistance and has been funded by the National Cancer Institute, the Leukemia and Lymphoma Society Translational Research Program and the Department of Veterans Affairs. Current resrach focuses on signal transduction pathways in acute myeloid leukemia with fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) and preclinical development of novel therapeutic approaches to acute myeloid leukemia with this common and prognostically unfavorable molecular abnormality. Finally, Dr. Baer has a long track record of mentoring students, residents, postdoctoral fellows and junior faculty.
Leukemia, drug resistance, cell signaling
Kapoor S, Natarajan K, Baldwin PR, Doshi KA, Lapidus RG, Mathias TJ, Scarpa M, Trotta R, Davila E, Kraus M, Huszar D, Tron AE, Perrotti D, Baer MR. Concurrent inhibition of Pim and FLT3 kinases enhances apoptosis of FLT3-ITD acute myeloid leukemia cells through increased Mcl-1 proteasomal degradation. Clin Cancer Res. 2018 Jan 1;24(1):234-247.
Perl AE, Altman JK, Cortes J, Smith C, Litzow M, Baer MR, Claxton D, Erba HP, Gill S, Goldberg S, Jurcic JG, Larson RA, Liu C, Ritchie E, Schiller G, Spira AI, Strickland SA, Tibes R, Ustun C, Wang ES, Stuart R, Röllig C, Neubauer A, Martinelli G, Bahceci E, Levis M. Slective inhibition of FLT3 by gilteritinib in relapsed or refractory acute myeloid leukemia: a multicenter, first-in-human, open-label, phase 1-2 study. Lancet Oncol. 2017 Aug;18(8):1061-1075.
Larrosa-Garcia M, Baer MR. FLT3 inhibitors in acute myeloid leukemia: Current status and future directions. Mol Cancer Ther. 2017 Jun;16(6):991-1001.
Doshi KA, Trotta R, Natarajan K, Rassool FV, Tron AE, Huszar D, Perrotti D, Baer MR. Pim kinase inhibition sensitizes FLT3-ITD acute myeloid leukemia cells to topoisomerase 2 inhibitors through increased DNA damage and oxidative stress. Oncotarget. 2016 Jul 26;7(30):48280-48295.
Gourdin TS, Zou Y, Ning Y, Emadi A, Duong VH, Tidwell ML, Chen C, Rassool FV, Baer MR. High frequency of rare structural chromosome abnormalities at relapse of cytogenetically normal acute myeloid leukemia with FLT3 internal tandem duplication. Cancer Genetics 207:467-73, 2014. Epub 2014 Sep 16.
Natarajan K, Xie Y, Burcu M, Linn DE, Qiu Y, Baer MR. Pim-1 kinase phosphorylates and stabilizes 130 kDa FLT3 and promotes aberrant STAT5 signaling in acute myeloid leukemia with FLT3 internal tandem duplication. PLoS One 8:e74653, 2013. Epub 2013 Sep 5.
Sen R, Natarajan K, Bhullar J, Shukla S, Fang H, Cai L, Chen Z-S, Ambudkar SV, Baer MR. The novel BCR-ABL and FLT3 inhibitor ponatinib is a potent inhibitor of the multidrug resistance-associated ATP-binding cassette transporter ABCG2. Molecular Cancer Therapeutics 11:2033-44; 2012.
Clinical Specialty Details
Leukemias, Myeloproliferative Neoplasms, Myelodysplastic Syndromes, Clinical Trials, Hematology