个人简介

Mark Levis, M.D., Ph.D., professor of oncology in the Division of Hematologic Malignancies at the Johns Hopkins University School of Medicine, co-directs the Hematologic Malignancies and Bone Marrow Transplantation Program at the Johns Hopkins Kimmel Cancer Center. Dr. Levis received his medical degree at the University of California, San Francisco, prior to completing his residency at Johns Hopkins, and completed fellowships in both oncology and medical oncology at Johns Hopkins as well. Dr. Levis’ laboratory research focuses on the development of molecularly-targeted therapies for leukemia. Currently, he is actively involved in the pre-clinical and clinical development of small molecule inhibitors of protein kinases, including FLT3. The research involves studying the biochemical effects of these inhibitors on samples taken from leukemia patients, with the broad goal of identifying and validating novel molecular therapeutic targets in these hematopoietic malignancies. While Dr. Levis does play a key role in the pre-clinical development of these therapies, he is particularly interested in translating this research to the bedside of his patients by using correlative studies to incorporate these novel therapies into existing treatments. In addition to his work in both the clinic and the laboratory, Dr. Levis has also published extensively in the top journals in his field, including Leukemia, Blood, and the New England Journal of Medicine. He has also been recognized as the Clinical Scholar of the Leukemia and Lymphoma Society. In addition to his role within the Kimmel Cancer Center, he serves on the faculty for the Johns Hopkins Graduate Training Program in Cellular and Molecular Medicine, a Ph.D. program that prepares scientists to conduct laboratory research at the cellular and molecular level that is designed to have a direct impact on the understanding of human diseases. MD, University of California San Francisco (1994)

研究领域

Kinase inhibitors; Targeting the FLT3 signaling pathway as a treatment for acute leukemia.

Our broad research goals are to identify and validate novel molecular therapeutic targets in hematopoietic malignancies. We are interested in the identification and pre-clinical development of novel targeted therapies, and, in particular, the “translational” step of this research by using correlative studies to incorporate these novel therapies into existing treatments. Our research is of particular interest to those who wish to be involved in directly translating the results of laboratory bench work into meaningful benefits for patients. Currently, we are actively involved in the pre-clinical and clinical development of small molecule kinase inhibitors targeting the FLT3 signaling pathway in acute myeloid leukemia. We are interested in 3 compounds in particular- AC220, a FLT3/KIT inhibitor; crenolanib,a selective FLT3 inhibitor with activity against resistant point mutations; and PLX3397, another inhibitor of KIT and FLT3. The active projects in the lab include: Characterization of cytotoxic responses of different hematologic malignancies to FLT3 and KIT kinase inhibition; Examination of the interaction of bone marrow stroma and stroma-derived cytokines on the efficacy of these inhibitors; Examination of the differential effect of FLT3 inhibition versus combined FLT3/KIT inhibition on acute myeloid leukemia and bone marrow progenitor cells; and Correlative laboratory studies using blood and marrow samples from patients treated with FLT3 inhibitors, with the aim of developing predictive models for clinical response.

近期论文

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Levis M, Tse K-F, Smith BD, Garrett E, Small D. A FLT3 tyrosine kinase inhibitor is cytotoxic to AML blasts harboring a FLT3/ITD mutation. Blood. 2001 Aug 1;98(3):885-7. Levis M, Brown P, Smith BD, Stine A, Pham R, Stone R, DeAngelo D, Galinsky I, Giles F, Estey E, Kantarjian H, Cohen P, Wang Y, Roesel J, Karp J, and Small D. Plasma inhibitory activity (PIA): A pharmacodynamic assay reveals insights into the basis for cytotoxic response to FLT3 inhibitors. Blood 2006 Nov 15;108(10):3477. PMC1895426 Sexauer A, Perl A, Yang X, Borowitz M, Gocke C, Rajkhowa T, Thiede C, Frattini M, Nybakken GE, Pratz K, Karp J, Smith BD, Levis M. Terminal myeloid differentiation in vivo is induced by FLT3 inhibition in FLT3/ITD AML. Blood. 2012;120(20):4205-14. PMCID: 3501718. Ravandi F, Alattar ML, Grunwald MR, Rudek MA, Rajkhowa T, Richie MA, Pierce S, Daver N, Garcia-Manero G, Faderl S, Nazha A, Konopleva M, Borthakur G, Burger J, Kadia T, Dellasala S, Andreeff M, Cortes J, Kantarjian H, Levis M. Phase 2 study of azacytidine plus sorafenib in patients with acute myeloid leukemia and FLT-3 internal tandem duplication mutation. Blood. 2013;121(23):4655-62. PMCID: 3674666. Cortes JE, Kantarjian H, Foran JM, Ghirdaladze D, Zodelava M, Borthakur G, Gammon G, Trone D, Armstrong RC, James J, Levis M. Phase 1 study of quizartinib administered daily to patients with relapsed or refractory acute myeloid leukemia irrespective of FMS-like tyrosine kinase 3-internal tandem duplication status. J Clin Oncol. 2013; 31(29):3681-7. PMCID: 3804291.