Reuben Kapur, PhD
Frieda and Albrecht Kipp Professor of Pediatrics
Dr. Kapur's laboratory focuses on understanding the mechanisms of childhood leukemias including acute myeloid leukemias, Juvenile myelomoncytic leukemias and pediatric bone marrow failure syndromes such as Fanconi Anemia and Diamond Blackfan Anemia. The ultimate goal of Dr. Kapur's work is to develop novel therapies for the treatment of these diseases.
Titles & Appointments
- Professor of Biochemistry & Molecular Biology
- Professor of Medical & Molecular Genetics
- Professor of Microbiology & Immunology
- Director, Program in Hematologic Malignancies & Stem Cell Biology, Wells Center for Pediatric Research
- Co-Program Leader, Hematopoiesis & Heme Malignancy (HHM), Indiana University School of Medicine, Simon Cancer Center
My laboratory focuses on understanding the signaling pathways involved in regulating normal and abnormal hematopoiesis. Specifically, we are interested in understanding how PI3Kinase and its downstream targets including members of the Rho family GTPases including Rho associated kinase (ROCK) and Rap1 contribute to stem and progenitor cell functions and leukemia initiating cell functions. In the context of leukemogenesis, we are also interested in understanding the role of oncogenic forms of KIT and FLT3 receptors in regulating MPNs as well as AML, with the intent of defining novel therapeutic targets. More recently, we have begun to examine how cooperation between oncogenic receptors (mutants of receptor tyrosine kinases and non-receptor tyrosine kinases including phosphatases) and mutations in epigenetic regulators (Dnmt3a and Tet2) cooperate to result in AML and MPNs. Our lab uses pharmacologic, genetic and biochemical approaches including established as well as newly created mouse models including xenograft models of leukemogenesis that recapitulate the human disease to accomplish these goals. We recently discovered that P38alpha stress MAP Kinase pathway contributes to the recovery of hematopoietic stem and progenitor cells from anemia induced by hemolysis and chemotherapy drugs. Furthermore, we have shown that inhibition of P38 activity reverses cell death induced by down-regulation of a ribosomal protein subunit 19 or RPS19, which is found to be mutated in 25 percent of Diamond-Blackfan anemia patients, a disease that currently has no treatment as well as in cells bearing mutations in Fanconi Anemia. We are interested in defining the role of P38 pathway in stress hematopoiesis including Fanconi Anemia and identifying downstream targets of P38.
American Society for the Advancement of Science
American Society of Hematology
Golden Key Honors Society
Indiana University Simon Center
International Society for Experimental Hematology
Phi Beta Kappa Society