Academics:
Harvard Medical School, Postdoctoral Research in Cancer Biology and Genetics
University of Southern California, Ph.D. in Molecular Biology and Biochemistry
Purdue University, BS in Chemistry/Biochemistry
Research:
I have studied Ras driven tumors since 2002. Ras driven tumors are highly aggressive, malignant prone tumors that are associated with drug resistance. My research focus encompasses aberrant hyperactivation of Ras through two mechanisms: constitutive oncogene activation and loss of tumor suppressor-mediated inhibition of Ras. Both mechanisms lead to uncontrolled Ras signaling and uncontrolled cell proliferation.
Neurofibromin and the epidermal growth factor receptor family are two main areas of active research. Neurofibromin (NF1) is a RasGAP associated with the familial genetic predisposition syndrome, Neurofibromatosis Type 1. The epidermal growth factor receptor family (EGFR) includes four receptor tyrosine kinases (EGFR, HER2, ErbB3, ErbB4) frequently genetically mutated leading to constitutive signaling associated with many aggressive tumor types. The role of CDKN2A, p53 and PTEN often cooperate with these described tumor types and are also part of our research focus on Schwann cell biology in the peripheral nervous system (PNS). In cancer, tumor suppressors are lost, and oncogenes are hyperactivated.
Bioinformatics is a main tool used in the lab to understand the genomic and transcriptomic profiles of these cancer types. We use this analysis, along with in vitro and in vivo models to develop therapeutic targets to inhibit cancer cell growth.
We are beginning to explore the distinct roles different NF1 and Ras protein isoforms play in the central nervous system (CNS).