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Rebecca J. Chan MD PhD

E-mail: rchan@iupui.edu
Phone: 317-274-4719
Office: R4 170

Rebecca J. Chan, MD, PhD

Associate Professor of Pediatrics

Associate Director, Indiana University MSTP 

Primary Appointment: Department of Pediatrics

Joint Appointment: Department of Medical & Molecular Genetics

Education

  • Research Fellowship: Indiana University School of Medicine, Indianapolis, IN
  • Internal Medicine Residency: UCLA Medical Center, Los Angeles, CA
  • MD: Indiana University School of Medicine, Indianapolis, IN
  • PhD: Indiana University School of Medicine, Indianapolis, IN

Research Interest:

To understand the etiology of phenotypic abnormalities found in Noonan syndrome, juvenile myelomonocytic leukemia, and acute myeloid leukemia. Noonan syndrome is a common (1 in 1500 to 2500 live births) autosomal dominant disorder characterized by dysmorphic facial features, congenital heart malformations, and a variety of hematologic abnormalities including a predisposition to juvenile myelomonocytic leukemia (JMML). Mutations in the human PTPN11 locus, which encodes for the protein tyrosine phosphatase, Shp2, have been identified in 50% of Noonan syndrome patients. Energetics-based functional analysis of mutant Shp2 proteins observed in Noonan syndrome patients predict increased phosphatase activity, suggesting that gain-of-function Shp2 mutations may account for the abnormalities observed in Noonan syndrome and JMML. Additionally, Shp2 expression is commonly upregulated in acute myeloid leukemia (AML), and Shp2 functions in collaboration with FLT3-ITD to promote AML and with oncogenic KIT to promote systemic mastocytosis.

As such, the Chan laboratory is focused on the role of the protein tyrosine phosphatase, Shp2, in childhood myeloid leukemias including oncogenic Shp2-induced juvenile myelomonocytic leukemia (JMML), FLT3-ITD-induced acute myeloid leukemia (AML), and oncogenic KIT-induced systemic mastocytosis (SM). Our long-term goals are to utilize genetic methods to dissect the aberrantly regulated signaling pathways involving Shp2 in an effort to define novel therapeutic targets in myeloid malignancies.

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