Benjamin L. Ebert
Department of Medicine
Karp Building, CHRB 5.210
75 Francis Street
Boston, MA 02115
Visit my lab page here.
We study the biology and treatment of cancer using hematopoiesis as a model system. The laboratory employs a range of genomic technologies as well as classical cellular and molecular biology approaches to investigate the biology of specific human diseases, particularly hematopoietic malignancies and disorders of red blood cell production.
A major focus of the laboratory is the myelodsyplastic syndrome (MDS), a pre-malignant disorder of hematopoietic stem cells that progresses to acute leukemia. In recent work, we identified a gene that plays a central role in the pathophysiology of the 5q- syndrome, a subtype of MDS. Our findings revealed a molecular link between the 5q- syndrome and congenital bone marrow failure syndromes such as Diamond Blackfan Anemia.
We are also actively involved in the identification and development of small molecules that could be useful for the treatment of cancer and hematologic disorders. We are studying compounds that induce fetal hemoglobin and could be useful for the sickle cell anemia. In addition, we are working on the identification and characterization of compounds that alter hematopoietic differentiation that could be useful for the treatment of cancer and non-malignant hematopoietic disorders.
Bejar R, Stevenson K, Abdel-Wahab O, Galili N, Nilsson B, Garcia-Manero G, Kantarjian HM, Raza A, Levine R, Neuberg D, Ebert BL. The Clinical Impact of Point Mutations in Myelodysplastic Syndromes. New England Journal of Medicine. 2011; 364: 2496-506.
Novershtern N, Subramanian A, Lawton LN, Mak RH, Haining WN, McConkey ME, Habib N, Yosef N, Chang CY, Shay T, Frampton GM, Drake AC, Leskov I, Nilsson B, Preffer F, Dombkowski D, Evans JW, Liefield T, Smutko JS, Chen J, Friedman N, Young RA, Golub TR, Regev A, Ebert BL. Densely interconnected transcriptional circuits control cell states in human hematopoiesis. Cell 2011; 144: 296-309.
Dutt S, Narla A, Lin K, Mullally A, Abayasekara N, Megerdichian C, Wilson FH, Currie T, Khanna-Gupta A, Berliner N, Kutok JL, Ebert BL. Haploinsufficiency for ribosomal protein genes causes selective activation of p53 in erythroid progenitor cells. Blood 2011;117:2567-76.
Bradner J, Mak R, Tanguturi SK, Mazitschek R, Haggarty SJ, Ross K, Chang CY, Bosco J, West N, Morse E, Lin K, Shen JP, Kwiatkowski NP, Gheldof N, Dekker J, DeAngelo DJ, Carr SA, Schreiber SL, Golub TR, Ebert BL. A Chemical Genetic Strategy Identifies HDAC1 and HDAC2 as Therapeutic Targets in Sickle Cell Disease. Proc Natl Acad Sci 2010; 107:12617-22.
Mullally A, Lane SW, Ball B, Megerdichian C, Okabe R, Al-Shahrour F, Paktinat M, Haydu JE, Housman E, Lord AM, Wernig G, Kharas M, Mercher T, Kutok J, Gilliland DG, Ebert BL. Physiological Jak2V617F Expression Causes a Lethal Myeloproliferative Neoplasm with Differential Effects on Hematopoietic Stem and Progenitor Cells. Cancer Cell 2010; 17:584-96.
For a complete listing of publications click here.
Last Update: 7/26/2012