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Kiran  Mahajan

Kiran Mahajan

Kiran Mahajan
Assistant Professor


Phone: 813/745-4062


PhD, Indian Institute of Science, Bangalore, 1998
Postdoctoral Fellowship, Lineberger Cancer Center, UNC Chapel Hill, 1998-2004
Research Assistant Professor, Dept of Pharmacology, Lineberger Cancer Center, UNC Chapel Hill, 2004-2007
Research Scientist, Moffitt Cancer Center, 2007-2015
Assistant Professor, Dept of Oncological Sciences, USF, 2011-current
Assistant Member, Moffitt Cancer Center, 2015-current


The overall goal of my research program is to identify and characterize novel epigenetic targets critical for the growth and metastasis of hormone refractory cancers using cancer stem cell models. Specifically, the first step is to delineate how histone modifications interact with other chromatin components to modulate distinct transcription programs in cancer and cancer stem cells (or tumor progenitor populations) to promote treatment resistance, ensure survival and effectively evade the cell death. Based on this fundamental knowledge the second step is to develop targeted therapies for these reversible modifications in the form of small molecule inhibitors.

Project 1: Tyrosine kinases have the ability to modify the chromatin directly as well as regulate the activity of chromatin modifiers to modulate gene expression programs (Mahajan K et. al., Nature Structural & Molecular Biology, 2012; and Mahajan K et. al., JBC, 2014). Working in collaboration with Dr. Lawrence laboratory, we have recently identified several small molecule inhibitors with potent in vitro inhibitory activity and anti-tumor activities (Lawrence H, Mahajan K et. al., J Med Chem, 2015). Our laboratory will characterize the efficacy and potency of the novel tyrosine kinase inhibitors and novel epigenetic inhibitors using tamoxifen-resistant breast tumor models and castration resistant prostate cancer models, to advance them as novel therapeutics for breast cancer and prostate cancer.

Project 2: Chromatin replication, the coordinate doubling of DNA and histones during each cell division, is a tightly regulated process, and represents one of the most vulnerable stages in cell cycle. Improper chromatin duplication in normal cells results in insidious genome instability and is manifested as cancer and developmental disorders. Conversely, targeted inhibition of proteins regulating chromatin duplication is often utilized as a strategy to induce mitotic catastrophe to eradicate proliferating cancer cells. Our recent discovery that WEE1 kinase directly phosphorylates, the core histone H2B at tyrosine 37(Y37), provides novel insights into pathways regulating chromatin duplication. Our lab will investigate the role of WEE1 epigenetic activity in cancer stem cell biology.