Goutam Chakraborty, PhD

Research Associate

Lab Phone





PhD, National Centre for Cell Science, Pune, India; MS, Darjeeling Government Collage, Univ. of North Bengal, India

In spite of significant progress toward early detection and treatment, once prostate cancer become refractory to anti androgen therapy and metastatic, it cannot be effectively cured. Current treatments include removal of the prostate, chemotherapy, radiotherapy, and anti-androgen drugs that could treat localized prostate cancer more effectively, a major stumbling block is that the tumors often recur.  When this second tumor arises, it typically no longer responds to anti-androgen therapy, and therefore is likely to metastasize and ultimately become untreatable.  When this happens, the cancer is called Androgen independent prostrate cancer (AIPC) and is the most lethal form of prostate cancer because it has high rates of metastasis and is therefore associated with poor prognosis. The origin and growth of this type of cancer is unknown, and it is of critical importance to understand how a benign lesion can become cancerous, invade the surrounding tissue, and eventually become insensitive to anti-androgen treatments. My overarching interests are in the mechanisms, which involved in progression of castration resistance prostate cancer (CRPC).


Gao H*, Chakraborty G*, et al Multi-organ Site Metastatic Reactivation Mediated by Non-canonical Discoidin Domain Receptor 1 Signaling. Cell 2016,166 (1), 47-62  (*Co 1st author).

Chakraborty G, Gadiya M et al. Inactivation of neogenin promotes castration resistance and bone metastasis in prostate cancer models. 106th Annual Meeting of the American Association for Cancer Research (AACR) 2015. Philadelphia. PA

Gao H, Chakraborty G, et al. Forward genetic screens in mice uncover mediators and suppressors of metastatic reactivation. Proc Natl Acad Sci U S A. 2014; 111(46): 16532-7.

Gao H, Chakraborty G, et al. The BMP Inhibitor Coco Induces Breast Cancer Cells to Undergo Reactivation at Lung Metastatic sites. Cell 2012; 150(4): 764-79.