Goutam Chakraborty, PhD

Goutam Chakraborty, PhD, is an Assistant Professor in the Department of Urology and Center of Excellence for Prostate Cancer at Tisch Cancer Institute in Icahn School of Medicine at Mount Sinai. Dr. Chakraborty’s research focuses on DNA damage repair (DDR), cancer metabolism, cell biology, cell signaling pathways, metastasis, and cancer stem cells. The success of Dr. Chakraborty’s interdisciplinary research activity is demonstrated by peer-reviewed publications in high-impact journals such as Cell, Cancer Cell, Journal of Clinical Investigation, Clinical Cancer Research, Proceedings of the National Academy of Sciences of the United States of America, Cancer Research, and more.

Education:

M.Sc Darjeeling Government College (North Bengal University), Darjeeling, India
Ph.D: National Centre for Cell Science, Pune, India
Postdoctoral Fellowship: Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY

Recent Publications

1. Chakraborty G, Patail NK, Hirani R, Nandakumar S et. al. Attenuation of SRC kinase activity augments PARP inhibitor–mediated synthetic lethality in BRCA2-altered prostate tumor. Clin Cancer Research; 2021 Mar 15;27(6):1792-1806
2. Chakraborty G, Armenia J, Mazzu YZ, Nandakumar S, et. al Significance of BRCA2 and RB1 Co-loss in Aggressive Prostate Cancer Progression. Clin Cancer Res. 2020 Apr 15;26(8):2047-2064.
3. Su W, Han HH, Wang Y, Zhang B, Zhou B, Cheng Y, Rumandla A, Gurrapu S, Chakraborty G, et. al. The Polycomb Repressor Complex 1 Drives Double-Negative Prostate Cancer Metastasis by Coordinating Stemness and Immune Suppression. Cancer Cell. 2019 Aug 12;36(2):139-155
4. Komura K, Yoshikawa Y, Shimamura T, Chakraborty G, Gerke TA, et. al. ATR inhibition controls aggressive prostate tumors deficient in Y-linked histone demethylase KDM5D. J Clin Invest. 2018 Jul 2;128(7):2979-2995
Complete List of the Published Work:
https://www.ncbi.nlm.nih.gov/myncbi/1TuL65ueTfOQs/bibliography/public/

Editorials and Commentary on the research articles

Attenuation of SRC Kinase Activity Augments PARP Inhibitor-Mediated Synthetic Lethality in BRCA2-Altered Prostate Tumors - Beyond the Abstract
https://www.urotoday.com/recent-abstracts/urologic-oncology/prostate-cancer/130327

Double Trouble: Concomitant RB1 and BRCA2 Depletion Evokes Aggressive Phenotypes.
https://clincancerres.aacrjournals.org/content/26/8/1784

"BRCA2 and RB1 loss responds to PARP inhibitors." Nature Reviews Urology, vol. 17, no. 3,
https://www.nature.com/articles/s41585-020-0293-0

Doubling down on tumor suppressor deletion.
https://www.science.org/doi/10.1126/scitranslmed.aba2903

Honors and awards

2019 Young Investigator Award, Prostate Cancer Foundation
2018 Speaker, 12th Annual Multi-institutional Prostate Cancer Program Retreat
2015 Plenary Speaker, 1st International Conference on Translational Research: From Basic Science to Clinical Application, KIIT University, Bhubaneswar, India
2015.   Presentation Award, 8th Annual Multi Institutional Prostate Cancer Program Retreat.
2014.   Presentation Award, Postdoctoral Research Symposium, MSKCC
2013 Plenary Speaker, 13th International Conference on Cancer Related Bone Disease, Miami,
2012 Postdoctoral Training Award, Department of Defense Prostate Cancer Research Program.
2007    Young Investigator Award, Society for Free Radical Research-Asia.

Current Funding Supports

Prostate Cancer Foundation
Department of Defense Prostate Cancer Research Program

Research Interest:

DNA damage repair (DDR) deficiency and lethal prostate cancer: Unlike many cancers driven by a small number of hotspot mutations, prostate cancer is driven more by somatic copy number alteration (CNA), which affects large segments of chromosomes. Since CNA burden is associated with DDR alteration, therefore, DDR pathway alterations are more frequent in lethal prostate cancer than previously reported. The prevalence of germline and somatic mutations in BRCA2, a hallmark DDR gene, are significantly increased in metastatic castration-resistant PC (mCRPC) compared to localized PC. We are investigating the molecular insights of BRCA2/DDR alterations in prostate cancer biology for consideration of DDR alteration as the master driver of the transformation from indolent, localized prostate cancer to lethal mCRPC.
Overcoming PARP inhibitor resistance: Cancer cells with alterations in DDR genes are hypersensitive to drugs that inhibit PARP. These findings led to the recent FDA approval of PARP inhibitors for patients with several cancer types, though the effects are not durable. Our research has focused on uncovering mechanisms of resistance to PARP inhibitors, with the ultimate goal of identifying therapeutic strategies to overcome this resistance and developed rational for future clinical trials.
Metabolism, genetic abnormalities and cancer progression: Despite the many recent efforts, the metabolic reprogramming of cancer cells is far from fully characterized primarily because of our lack of knowledge on how a genetic abnormality turns on or reprograms a metabolic switch in cancer cells. Our research focuses on the interplay between clinically relevant genetic mutations and the rewriting of the metabolic pathways in cancer cells, thereby identifying targetable molecular pathways to reduce the cancer burden.
Y-Chromosome and cancer: Cancer affects men and women differently. Much of the sex difference in cancer rates is due to lifestyle factors, especially smoking, which historically has been more common in men. But even some cancers that are not known to be linked to lifestyle tend to appear more often in men. We will undertake an innovative research approach to ask why. The focus of our efforts is the most fundamental difference between men and women: the Y chromosome. Though loss of the Y chromosome (ChrY) in men has been associated with increased risk of cancer including prostate cancer and mortality, the role of ChrY genes in cancer progression is poorly understood. We are investigating the mutational landscape of ChrY and determine if the loss of Y-chromosome (LOY) is significantly associated with disease risk in men.