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Dr. Srikumar Chellappan

Professor and Chair
H. Lee Moffitt Cancer Center and Research Institute
12902 Magnolia Dr., Mail Code: SRB3

Brief Biography:

Dr. Chellappan obtained his Ph.D. in Biochemistry from the Indian Institute of  Science, Bangalore, India and did his post-doctoral training at Duke University Medical Center, Durham, NC. Subsequently, he went to become an Assistant Professor in the Department of Pathology at Columbia University in New York from 1992-2001. He joined Moffitt Cancer Center as an Associate Professor in 2001 and was promoted to Full Professor/Senior Member in 2006. He was recently named as the Chair of the new Department of Tumor Biology.

Dr. Chellappan’s research interests include signal transduction and transcriptional regulation, especially in the context of tumor progression and metastasis.  His laboratory has been focusing on the gene regulatory mechanisms in non-small cell lung cancer and how they can be targeted using novel drugs. His work has been published in journals like PNAS, Journal of Clinical Investigation, Molecular and Cellular Biology, Cancer Research etc. Dr. Chellappan has served on various NIH Study sections as well as site visit teams and was a Charter member of the Tumor Progression and Metastasis Study Section. He has also served on the editorial board of multiple journals including Molecular Pharmacology and Molecular Cancer.  His research has been continuously funded by the NIH since 1994.


Academic positions:

1991-1992 Research Assistant Professor, Dept. of Medicine, Duke University Medical Center, Durham, North Carolina.

1992-1999 Assistant Professor, Dept. of Pathology, College of Physicians and Surgeons, Columbia University, New York.

1999-2001 Assistant Professor of Clinical Pathology, College of Physicians and Surgeons, Columbia University, New York.

2001- 07/06 Associate Professor, Drug Discovery Program, Department of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.

08/2006 –  Senior Member, Drug Discovery Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL.

Professor, Dept. of Oncologic Sciences, University of South Florida   (Secondary)

Professor, Dept. of Molecular Medicine, University of South Florida. (Secondary)

11/2009- Scientific Director, National Functional Genomics Center, Moffitt Cancer Center.

03/2010- Chair, Dept. of Tumor Biology, Moffitt Cancer Center.


Research interests:

My laboratory was started in 1992 and our ongoing studies iaim to understand the role of the Rb-E2F cell cycle regulatory pathway as well as additional signaling pathways in promoting tumor growth,  angiogenesis and metastasis. This investigator was involved with the original study that demonstrated the physical interaction between the Rb protein and the E2F transcription factor (Chellappan et al., Cell 65, 1053-1061, 1991).  Since establishing my own laboratory at Columbia University, we have been studying how signals received at the cell surface contact the cell cycle regulatory pathways to elicit various responses like proliferation, differentiation, senescence and apoptosis. In this context, we made some discoveries that are highly relevant to the basic biology of cancer.  For example, we demonstrated that kinases like C-Raf, p38 and ASK1 can target the Rb protein and lead to its inactivation in a signal dependent manner.  Further, we observed that the binding of Raf-1 to Rb was elevated in human cancers and have developed small-molecule inhibitors of this interaction that appear to have potent anti-angiogenic and anti-cancer effects in vivo. During the course of these investigations, we observed that signals emanating from the nicotinic acetylcholine receptors target the Rb-E2F pathway leading to cell proliferation, enhanced angiogenesis, epithelial-mesenchymal transition and enhanced metastasis. One of the major efforts in my lab now is to elucidate the signaling pathways that mediated events downstream of nAChR signaling in NSCLC and pancreatic cancers. We have recently identified stem-like cells in cultured lung cancer cell lines and primary human tumors xenografted in mice. We have also succeded in developing small molecule inhibitors of cell cycle progression and tumor growth.


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