Anindya Bagchi, PhD - Sanford Burnham Prebys

Dr. Bagchi comes to Sanford Burnham Prebys from the University of Minnesota, where he has been since 2008, having earlier held positions as assistant professor of Cell Biology & Development (Genetic Mechanism of Cancer) and Co-Director of Mouse Genetics Laboratory at University of Minnesota. Dr. Bagchi brings his lab with him and an established research program in genetic mechanisms of cancer. He completed his PhD degree at Jawaharlal Nehru University in New Delhi, India and then worked as a postdoctoral fellow at the Cold Spring Harbor Laboratory in New York. He has been an American Cancer Society Research Scholar since 2014 and Masonic Scholar since 2010.

Related Disease
Cancer

My lab studies the genetic mutations that drive cancer. I am a geneticist by training, and I am passionate about finding the hidden drivers of cancer. As a research community, we have made tremendous progress in the last few decades in understanding the nature of the beast, but now is the time to translate those knowledge to actionable interventions. A riveting idea that has excited us for sometime is to illuminate the genetic mutations which act as life line to many cancers. This would expose their Achilles heel that we can exploit in near future to develop new forms of treatment. That is what my lab’s work is focused on. We have identified and characterized several key mutations that we have shown as proof of concept can be targeted in as much as 30% of all cancers. The focus of the lab is now to carry out experiments that will allow us to develop this work beyond the proof of concept, ideally to successful clinical trials.

Select Publications

Showing 3 of 3

PVT1 dependence in cancer with MYC copy-number increase.

Tseng YY, Moriarity BS, Gong W, Akiyama R, Tiwari A, Kawakami H, Ronning P, Reuland B, Guenther K, Beadnell TC, Essig J, Otto GM, O’Sullivan MG, Largaespada DA, Schwertfeger KL, Marahrens Y, Kawakami Y, Bagchi A

Nature 2014 Aug 7 ;512(7512):82-6

CHD5 is a tumor suppressor at human 1p36.

Bagchi A, Papazoglu C, Wu Y, Capurso D, Brodt M, Francis D, Bredel M, Vogel H, Mills AA

Cell 2007 Feb 9 ;128(3):459-75

Loss of HIF1A From Pancreatic Cancer Cells Increases Expression of PPP1R1B and Degradation of p53 to Promote Invasion and Metastasis.

Tiwari A, Tashiro K, Dixit A, Soni A, Vogel K, Hall B, Shafqat I, Slaughter J, Param N, Le A, Saunders E, Paithane U, Garcia G, Campos AR, Zettervall J, Carlson M, Starr TK, Marahrens Y, Deshpande AJ, Commisso C, Provenzano PP, Bagchi A

Gastroenterology 2020 Nov ;159(5):1882-1897.e5

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PVT1 dependence in cancer with MYC copy-number increase.

CHD5 is a tumor suppressor at human 1p36.

Loss of HIF1A From Pancreatic Cancer Cells Increases Expression of PPP1R1B and Degradation of p53 to Promote Invasion and Metastasis.

Biography

Research

Select Publications

PVT1 dependence in cancer with MYC copy-number increase.

CHD5 is a tumor suppressor at human 1p36.

Loss of HIF1A From Pancreatic Cancer Cells Increases Expression of PPP1R1B and Degradation of p53 to Promote Invasion and Metastasis.