Dr. Pinki Chowdhury
University of Michigan, Cancer Center, Ann Arbor, Michigan, USA
2002-2003: Guest Lecturer in Microbiology (Undergraduate) under The University of Calcutta, Kolkata, India. 2003 - 2005: Junior Research Fellow (DBT, Govt. of India), Kolkata, India. April 2005 - June 2009: Graduate Research Fellow (CSIR-UGC NET, Govt. of India) for PhD degree, Kolkata, India. 2009 - 2010: Post-doctoral fellow under Dr. Ferid Murad (Nobel Laureate, 1998 in Medicine), Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas, USA. 2010 ? 2014: Post-doctoral Associate, Department of Internal Medicine (Hematology & Oncology), Baylor College of Medicine, Houston, Texas, USA. 2015- present: Postdoctoral Research Associate, Department of Internal Medicine (Hematology & Oncology), University of Michigan Cancer Center, Ann Arbor, Michigan, USA.
Presently I?m working on ?Targeting the transcription factor in T-cell lymphomas: A novel therapeutic strategy to overcome chemotherapy resistance?. Peripheral T-cell lymphomas (PTCL), which account for ?15% of non-Hodgkin lymphomas (NHL) in North America, are poorly understood and associated with dismal outcomes. We observed that few GATA-family transcription factors classically associated with Th2 differentiation in conventional T cells is highly expressed in a molecularly and clinically distinct subset of PTCL. In cancer biology, the epigenetic landscape controls gene expression and determines cell lineage and ontogeny. Therefore, it is the repertoire of active enhancers within a cell that controls cell lineage and differentiation, and reflects cell ontogeny. GATA factors bind to T helper cells type 2 (Th2) associated genes (e.g. cytokines) and upregulate their expression in PTCL, suggesting that this TCL subset are Th2 derived. ChIP-seq technology has been implicated to identify GATA binding sites in these TCL and characterize their enhancer landscape. Furthermore, the precise impact of most post-translational modifications on GATA factor activities, including chromatin occupancy, coregulator recruitment, GATA switches and higher order chromatin transitions at endogenous loci is still unknown. . Therefore, my ongoing interest is based on examining the extent to which clinically available HDAC inhibitors increase GATA acetylation (post-translational modification) and inhibit binding to its gene targets.
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