COLLEGE OF SCIENCE,
ENGINEERING AND
TECHNOLOGY
Assistant Professor
SB 203H | (713) 313.7219
Cassimereek@tsu.edu
Curriculum Vitae

Education and Training

  • Ph.D. 2008 (Purdue University, West Lafayette IN)
  • Post-Doctoral Research 2009-2013 (University of Texas Health Science Center, Houston TX)

Research Interests

The major focus of my research lab is to investigate the role of antioxidants in the sensitization of cancer cells to combinatory chemotherapeutic and plant-derived compounds. Through the use of dose response assays and molecular biology techniques, we aim to identify novel approaches to target tumors that become resistant to current cancer treatments.

Select Publications

Cassimere EK, Mauvais C, Denicourt C. p27kip1 is required to mediate a G1 cell cycle arrest downstream of ATM following genotoxic stress. PLoS One. (2016) Sep 9;11(9):e0162806.

Kumari A, Iwasaki T, Pyndiah S, Cassimere EK, Palani CD, Sakamuro D. Regulation of E2F1-induced apoptosis by poly(ADP-ribosyl)ation. Cell Death and Differentiation (2015) 22(2) 311-322

Castle CD, Cassimere EK, and Denicourt C.  Las1L interacts with the mammalian Rix1 complex to regulate ribosome biogenesis. Molecular and Cellular Biology (2012) 23:716-728

Lundgaard G.L., Daniels N.E., Pyndiah S., Cassimere E.K., Ahmed K.M., Rodrigue A., Kihara D., Post C.B., Sakamuro D.  Identification of a novel effector domain of BIN1 required for cancer suppression.  Journal of Cellular Biochemistry. (2011); 112(10):2992-3001

Pyndiah S., Tanida S., Ahmed K.M., Cassimere E.K., Choe C., and Sakamuro D.  c-Myc suppresses BIN1 to release Poly(ADP-Ribose) Polymerase1: A mechanism by which cancer cells acquire cisplatin resistance.  Science Signaling (2011); (166):ra19

Castle C.D, Cassimere E.K., Lee J. and Denicourt C.  Las1L is a nucleolar protein involved in ribosome biogenesis.  Molecular and Cellular Biology (2010); 30(18): 4404-4414

Cassimere E.K., Pyndiah S. and Sakamuro D.  The c-Myc-interacting pro-apoptotic tumor suppressor BIN1 is a transcriptional target for E2F1 in response to DNA damage.  Cell Death and Differentiation (2009) 16(12):1641-1653

Kinney, E.L., Tanida, S., Rodrigue, A.A., Johnson, J.K., Tompkins, V.S. and Sakamuro, D. Adenovirus E1A oncoprotein liberates c-Myc activity to promote cell proliferation through abating Bin1 expression via Rb inactivation. Journal of Cellular Physiology (2008) 216(3): 621-631