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Radiation Medicine




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Photo of Vivek Rangnekar Vivek M. Rangnekar, Ph.D.
Professor and Alfred Cohen Chair in Oncology Research
Associate Director, Markey Cancer Center
Markey Program Co-Leader, Cancer Biology & Signaling

Combs Research Building
744 Rose Street 326
Lexington, KY 40536
Phone: (859) 257-2677


  • Cancer
  • Apoptosis
  • Tumor Suppressors
  • Molecular and Chemical Biology


  • B.S., University of Bombay, 1976
  • M.S., University of Bombay, 1979
  • Ph.D., University of Bombay, 1983
  • Post-doctoral Training, University of Chicago 1983-1986


NIH/NCI R21 CA179283 (PI: Rangnekar, VM) 04/01/14-03/31/16
“Regulation of Par-4 Secretion in Normal Cells for Paracrine Action in Tumor Cells ”
Goals: The objective of this project is to study the paracrine anti-cancer effect of Par-4 secretion by normal cells.

NIH/NCI R01 CA165469 (Multi-PI: Bondada, S; Rangnekar VM) 02/07/13-01/31/18
“Role of Tcl1 and Par-4 in regulation of chronic lymphocytic leukemia”
Goal: Determine the importance of BCR signaling and the role of specific SFKs in the regulation of Tcl-1 and Par-4 expression using the Tcl-1 mouse model of CLL. This will involve preclinical studies to test the efficacy of extracellular Par-4/SAC to inhibit CLL growth. Role: Multi-PI.

NIH/NCI R01 CA060872 (PI: Rangnekar, VM) 09/30/95-04/30/14
“Mechanism of Apoptosis and Inhibition of Tumor Progression and Metastasis by Par-4”
Goals: The goal of this proposal is to study the mechanism of apoptosis induced by Par-4 in prostate cancer cells and animal models.
Role: PI

NIH/NCI T32 CA165990 (Multi-PI: Rangnekar, VM and Evers, BM) 04/01/13-03/31/16
“Interdisciplinary Research Training in Cancer Biology”
Goals: This project is to train pre-doctoral students and post-doctoral scholars in cancer biology. Role: Multi-PI.

NIH/NCI P30 CA177558 (PI: Evers, BM) 07/01/13-06/30/18) “University of Kentucky Markey Cancer Center – Cancer Center Support Grant” Goals: To obtain NCI Cancer Center designation. Role: Program Co-leader, Cancer Cell Biology and Signaling

CCTS UK Drug Discovery Grant (PI: Rangnekar, VM) 09/01/2013-08/31/2014
“Development of Vimentin Inhibitors for Secretion of Par-4 and Suppression of Tumor Metastasis” Goals: To identify arylquinoline derivatives that induce robust secretion of Par-4. Role: PI

The Edward P Evans Foundation (PI: Van Zant, G) 04/01/12-03/30/17
“Molecular Mechanisms and Therapies for Radiation-Induced Myelodysplastic Syndrome (MDS)”
Goals: Study the Molecular Mechanisms and Therapies for Radiation-Induced Myelodysplastic Syndrome (MDS). Role: Co-Investigator


Book Edition                    
Programmed Cell Death: Cellular and Molecular Mechanisms(volume 1) and Role in Disease, Pathogenesis & Prevention (volume 2). (Elsevier Science, Inc., NY). Editors: M. P. Mattson, S. Estus, and V. M. Rangnekar. January 2001.

Recent Book Chapters 
K. M. Vasudevan, P. Ranganathan, and V. M. Rangnekar (2005) Regulation of Par-4 by oncogenic Ras.  Methods in Enzymology.  (Elsevier Science, Inc., NY). Editors: Bill Balch, Channing Der and Alan Hall. Volume 407, pp. 422-442.

N. Shukla, N. Hebbar and Vivek M. Rangnekar (2012) Par-4 in prostate cancer in Prostate Cancer: Biochemistry, Molecular Biology and Genetics (Springer Science) Editor: Don Tindall (Mayo Clinic). pp. 481-495.

Selected Articles
A. Goswami, R. Burikhanov, A. de Thonel, N. Fujita, M. Goswami, Y. Zhao, J. E. Eriksson, T. Tsuruo, and V. M. Rangnekar (2005) Binding and phosphorylation of Par-4 by Akt is essential for cancer cell survival.  Molecular Cell 20: 33–44.

A. Goswami, P. Ranganathan and V. M. Rangnekar (2006) The PI3K-Akt1-Par-4 Axis: A Cancer-Selective Therapeutic Target.  Cancer Res. 66, 2889-2892.

Y. Zhao, R. Burikhanov, S. Qiu, S. M. Lele, C. D. Jennings, S. Bondada, B. Spear, and V. M. Rangnekar (2007) Cancer resistance in transgenic mice expressing the SAC module of Par-4. Cancer Res. 67: 9276-9285.

K. M. Vasudevan, R. Burikhanov, A. Goswami, and V. M. Rangnekar (2007) Suppression of PTEN expression is essential for antiapoptosis and cellular transformation by oncogenic Ras. Cancer Res. 67: 10343-10350.

A. Goswami, S. Qiu, T. S. Dexheimer, P. Ranganathan, R. Burikhanov, Y. Pommier and V. M. Rangnekar. (2008) Par-4 binds to topoisomerase 1 and attenuates its DNA relaxation activity. Cancer Res. 68: 6190-6198.

R. Burikhanov, Y. Zhao, A. Goswami, S. Qiu, S. R. Schwarze, and V. M. Rangnekar. (2009) The tumor suppressor Par-4 activates an extrinsic pathway for apoptosis.  Cell 138: 377-388.

T.  Bhattarai and V. M. Rangnekar (2010) Cancer-selective apoptotic effects of extracellular and intracellular Par-4. Oncogene 29: 3873–3880.

Y. Zhao, R. Burikhanov, J. Brandon, S. Qiu,  B. J. Shelton, B. Spear,  S. Bondada,  S. Bryson and V. M. Rangnekar (2011) Systemic Par-4 inhibits metastatic tumor growth. Cancer Biol Ther. 12: 152-157.                                 

G.W.Warren, M. Romano, M.R. Kudrimoti, M.E. Randall, R.M. McGarry, A.K. Singh, and V.M. Rangnekar. (2012) Nicotinic modulation of therapeutic response in vitro and in vivo. Int. J. Cancer 131:2519-2527.

R. Burikhanov, T. Shresta-Bhattarai, S. Qiu, N. Shukla, N. Hebbar, S. Lele, C. Horbinski, and V. M. Rangnekar (2013) Novel mechanism of apoptosis resistance in cancer mediated by extracellular PAR-4. Cancer Res. 73:1011-1019.

T. Shrestha-Bhattarai, N. Hebbar, and V.M. Rangnekar (2013) Par(-4)oxysm in Breast Cancer. Cancer Cell 24(1):3-5.

R. Burikhanov, T. Shrestha-Bhattarai, N. Hebbar, S. Qiu, Y. Zhao, G. Zambetti, and V. M. Rangnekar (2014) Paracrine apoptotic effect of p53 mediated by tumor suppressor Par-4. Cell Reports.  

R. Burikhanov, T. Shrestha-Bhattarai, N. Hebbar, S. Qiu, Y. Zhao, G. Zambetti, and V. M. Rangnekar (2014) Paracrine apoptotic effect of p53 mediated by tumor suppressor Par-4. Cell Reports 6: 1–7.


Patent # 7,786,275, on August, 31 2010, to Vivek M. Rangnekar (radiation medicine) for "Identification of a unique core domain of Par-4 sufficient for selective apoptosis induction in cancer cells."

Provisional Patent filed on November 2013: Case # 13/1947 Arylquinoline and arylbenzopyran compounds and use of such to treat cancer.

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