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Nupam  Mahajan

Nupam Mahajan

Nupam Mahajan
Associate Professor

Contact

Office:
Phone: 813/745-4078
Email: Nupam.Mahajan@moffitt.org

Education

PhD, Indian Institute of Science, India, 1997
Postdoctoral Fellowship, University of North Carolina, Chapel Hill, NC, 1997-2004M
Assistant Professor, University of North Carolina, Chapel Hill, NC, 2004-2006

Research

A major interest in our lab is to determine how tyrosine phosphorylation regulates epigenetic processes that affect cellular homeostasis and cancer cell survival. We employ multiple tyrosine kinases to investigate these processes.

The two major examples are:
WEE1: As an epigenetic modulator
ACK1: Oncogene in prostate, breast, lung and pancreatic cancers

Some of the major findings of our lab include:

1) We demonstrated for the first time that WEE1 kinase is an epigenetic modifier; it phosphorylated histone H2B at Tyrosine 37 specifically in late S phase of cell cycle

2) H2B Tyr37-phosphorylation suppressed transcription of all core and linker histones, maintaining equimolar ratio of DNA to histones at the end of S phase

3) We demonstrated that ACK1 activation is present in various tumors, including prostate, breast, lung and pancreatic cancer.

4) We developed a novel ACK1-specific small molecule inhibitor. The `addiction to Ack1 signaling' was validated by small molecule inhibitor, which not only inhibited ACK1 signaling but also suppressed cancer cell growth

5) We identified a novel phosphorylation site, Tyrosine 176, in AKT, mediated by ACK1 kinase. AKT Tyr176- phosphorylation correlated with breast, prostate and pancreatic cancer progression to metastatic stages

6) Androgen receptor (AR) was identified to be ACK1 substrate; ACK1 phosphorylated AR at Tyr267, which initiated a distinct transcriptional program that was critical for castration resistant prostate cancer (CRPC)

7) We generated Ack1 transgenic mice that develop prostatic intraepithelial neoplasia (PINs)

8) We have generated Ack1 knockout mice

Current Projects:
a) WEE1 epigenetic signaling in cancer (melanoma and Glioblstoma)
b) Characterization of ACK1 knockout mice to assess ACK1-AKT signaling
c) Characterization of novel ACK1 inhibitor
d) Role of ACK1 in tamoxifen-resistance in breast cancer