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Robert Wang




My primary research interest is to uncover novel signaling pathways which may cross-link cellular transformation to cell quiescence or apoptosis. Ultimately, I expect to apply the understanding of intracellular signaling controls to anticancer treatment and prevention by selective induction of apoptotic signaling pathways in transformed cells or restoration of signaling control to re-gain the control of cell growth.

Description of Research

My research interests are to pursue novel molecules functioning in a quiescent state of normal cells and in apoptosis of malignantly transformed cells and to build translational research as a bridge from basic research to clinical research and applications for anticancer therapeutics and prevention. The goal of my basic research is to have a better understanding of the control of human cancers through exploration of novel signaling pathways for regulating cellular transformation, quiescence, and apoptosis. The approach of my translational research is to build preclinical models that reflect the molecular basis of cancer etiology and progression and for studies of tumor biology and etiology. Through molecular classification of oncogene- or carcinogen-induced human cancer cells, the genetic and molecular changes will be utilized as elements to constitute unique, identifiable characteristics of signatures of precancerous and cancerous cells at all stages of cancer development. Based on the molecular signature of cancerous cells, we will be able to determine the stage of cancers and identify molecular targets for choosing agents that prevent cancer by interfering with the biological processes underlying cancer development. Through collaborations we expect to establish research programs with multi-disciplines to link basic molecular and cellular research to clinical studies that will benefit our society for anticancer prevention and treatment.

Current Projects: (1) Identifying the role of a new family of protein kinase SAMK/Krs (src-activated MBP kinase/kinase responsive to stress) and Krs1-derived kinases in modulating cell quiescence and apoptosis. (2) Identifying the proapoptotic role of oncogenic Ras in the selective apoptosis of cancerous cells induced by discriminating anticancer agents. (3) Determining the potency and molecular signatures of tobacco carcinogens in the development of human breast cancer cells.


Ph.D.: Molecular Biology/Oncogene- University of Virginia, Health Science Center (1990)


Choudhary S, Rathore K, Wang HC. FK228 and oncogenic H-Ras synergistically induce Mek1/2 and Nox-1 to generate reactive oxygen species for differential cell death. Anticancer Drugs. 2010 Oct;21(9):831-40.

Choudhary S, Rathore K, Wang HC. Differential induction of reactive oxygen species through Erk1/2 and Nox-1 by FK228 for selective apoptosis of oncogenic H-Ras-expressing human urinary bladder cancer J82 cells. J Cancer Res Clin Oncol. 2010 May 15.

Song X, Siriwardhana N, Rathore K, Lin D, Wang HC. Grape seed proanthocyanidin suppression of breast cell carcinogenesis induced by chronic exposure to combined 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and benzo[a]pyrene. Mol Carcinog. 2010 May;49(5):450-63.

Choudhary S, Wang HC. Role of reactive oxygen species in proapoptotic ability of oncogenic H-Ras to increase human bladder cancer cell susceptibility to histone deacetylase inhibitor for caspase induction. J Cancer Res Clin Oncol. 2009 Nov;135(11):1601-13.

Siriwardhana N, Wang HC. Precancerous carcinogenesis of human breast epithelial cells by chronic exposure to benzo[a]pyrene. Mol Carcinog. 2008 May;47(5):338-48.

Siriwardhana N, Choudhary S, Wang HC. Precancerous model of human breast epithelial cells induced by NNK for prevention. Breast Cancer Res Treat. 2008 Jun;109(3):427-41.

Choudhary S, Wang HC. Pro-apoptotic activity of oncogenic H-Ras for histone deacetylase inhibitor to induce apoptosis of human cancer HT29 cells. J Cancer Res Clin Oncol. 2007 Oct;133(10):725-39.

Choudhary S, Wang HC. Proapoptotic ability of oncogenic H-Ras to facilitate apoptosis induced by histone deacetylase inhibitors in human cancer cells. Mol Cancer Ther. 2007 Mar;6(3):1099-111.

Song P, Wei J, Wang HC. Distinct roles of the ERK pathway in modulating apoptosis of Ras-transformed and non-transformed cells induced by anticancer agent FR901228. FEBS Lett. 2005 Jan 3;579(1):90-4.

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