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Subrata Haldar, Ph.D.

Associate Professor

Research

Cancer cells forget to die by the ability to keep them away from committing suicide by a delicate cellular process called "Apoptosis." This ability of cancer cells to evade apoptosis or programmed cell death is one of the keys for their fight against attack from chemo- or radiation therapy. The focus of our research program is to find ways to make these cancer cells sensitive to suicide. Our long-term goal is to develop apoptosis inducing therapy for chemoresistant malignant tumors.

Bcl2 (B cell lymphoma and leukemia-2) gene is the founding member of a large family of inhibitors and activators of apoptosis. Bcl2-like proteins (Bcl-xL/Mcl-1) play an essential role in controlling apoptosis. Consequently, deregulation of these proteins can contribute to diseases, most notably to cancer. Despite a major research effort, how Bcl2-like proteins control apoptosis is still a highly debated topic. As phosphorylation is a common way of regulating protein function, the discovery of Bcl2 phosphorylation is a very intriguing observation. We are poised to understand how phosphorylation of Bcl-2/Bcl-xL can regulate the development of B-lymphocytes using transgenic model developed in the laboratory.

Another objective of our research program is to explore the basis for the endocrine treatment of human pancreatic cancer. Carcinoma of the pancreas is one of the most aggressive human malignancies, with an extremely poor prognosis. Irradiation and cytotoxic chemotherapy alone or in combination have only a minor influence on survival. Pancreatic cancer cells are usually resistant to conventional apoptosis-inducing agents. A new treatment strategy in handling pancreatic tumors is the use of endocrine treatment. In our laboratory, we have studied the effect of an endogenous estrogen metabolite 2-methoxyestradiol (2-ME) on programmed cell death in human pancreatic cancer cells. Using cDNA microarray analysis as well as preclinical animal model, our research will be directed towards unraveling the potential downstream effector of 2-ME triggered apoptotic signaling pathway in pancreatic cancer.

SELECTED REFERENCES:

Basu, A. and Haldar, S. (2003) Identification of a novel Bcl-xL phosphorylation site regulating the sensitivity of Taxol or 2-Methoxyestradiol induced apoptosis. FEBS Lett. 538: 41-47.

Basu, A., Das, M., Qanungo, S., Fan, X-U, Dubois, G. and Haldar, S. (2002) Proteasomal Degradation of Human Peptidyl Prolyl Isomerase Pin 1-Pointing Phospho Bcl2 towards Dephosphorylation. Neoplasia 4: 218 - 227.

Haldar, S., Basu, A. and Croce, C.M (1998) Serine-70 is one of the critical sites for drug-induced Bcl2 phosphorylation in cancer cells. Cancer Res. 58: 1609-1615.

Haldar, S., Jena, N. and Croce, C.M. (1995) Inactivation of Bcl2 by phosphorylation. Proc. Natl. Acad. Sci. USA 92 : 4507-4511.

Qanungo, S., Basu, A., Das, M. and Haldar, S. (2002) 2-Methoxyestradiol elicits mitochondria dependent apoptotic signaling in Pancreatic cancer cells. Oncogene. 21: 4149-4157.