A photo of Biplab DasGupta.

Biplab Dasgupta, PhD

  • Member, Division of Oncology
  • Professor, UC Department of Pediatrics

About

Biography

My research areas are cancer metabolism and brain tumors. Our work seeks to identify new metabolic targets that could lead to novel and innovative treatments for cancer. We are also examining the molecular links between cancer and diabetes.

I became interested in cancer research during my graduate research courses in biology. In one of my lab’s groundbreaking discoveries, we identified the energy sensor adenosine monophosphate-activated protein (AMP) kinase as an essential gene for glioblastoma pathology. This work was published in Nature Cell Biology. We also performed the first gene-metabolite interactome of diffuse intrinsic pontine glioma (DIPG).

I am honored to have received the Larry E. Kun Achievement in Excellence award, the TeamConnor Childhood Cancer Foundation award (2019) and the Outstanding Achievement Award from Cincinnati Children’s for Brain Tumor Research (2016). I have been a principal investigator for more than 11 years and began working at Cincinnati Children’s in 2009. Work in my laboratory has been continuously supported by grants from the National Institutes of Health and various private foundation grants.

We have published in many well-respected journals, including Nature Cell Biology, PNAS, Nature Communications, Cancer Cell, Cell Reports, Science Advances, Cell Stem Cell, Developmental Cell, Cancer Research, Clinical Cancer Research, Journal of Neuroscience, Neuro-Oncology, and Trends in Pharmacological Sciences, among others.

PhD: Indian Institute of Chemical Biology, Calcutta, 2003.

Postdoctoral Fellowship: Washington University School of Medicine, St. Louis.

Interests

Metabolism; cancer development

Research Areas

Experimental Hematology and Cancer Biology, Oncology, Cancer and Blood Diseases

Publications

Selected

AMPK in the brain: its roles in glucose and neural metabolism. Muraleedharan, R; Dasgupta, B. FEBS Journal. 2021.

Selected

Mechanisms of stearoyl CoA desaturase inhibitor sensitivity and acquired resistance in cancer. Oatman, N; Dasgupta, N; Arora, P; Choi, K; Gawali, MV; Gupta, N; Parameswaran, S; Salomone, J; Reisz, JA; Lawler, S; et al. Science advances. 2021; 7.

Selected

AMPK-Regulated Astrocytic Lactate Shuttle Plays a Non-Cell-Autonomous Role in Neuronal Survival. Muraleedharan, R; Gawali, MV; Tiwari, D; Sukumaran, A; Oatman, N; Anderson, J; Nardini, D; Bhuiyan, MA N; Tkac, I; Ward, AL; et al. Cell Reports. 2020; 32.

Selected

AMP kinase promotes glioblastoma bioenergetics and tumour growth. Chhipa, RR; Fan, Q; Anderson, J; Muraleedharan, R; Huang, Y; Ciraolo, G; Chen, X; Waclaw, R; Chow, LM; Khuchua, Z; et al. Nature Cell Biology. 2018; 20:823-835.

Selected

The transcription factor Olig2 is important for the biology of diffuse intrinsic pontine gliomas. Anderson, JL; Muraleedharan, R; Oatman, N; Klotter, A; Sengupta, S; Waclaw, RR; Wu, J; Drissi, R; Miles, L; Raabe, EH; et al. Neuro-Oncology. 2017; 19:1068-1078.

Selected

Evolving Lessons on the Complex Role of AMPK in Normal Physiology and Cancer. Dasgupta, B; Chhipa, RR. Trends in Pharmacological Sciences. 2016; 37:192-206.

Selected

Serine/Threonine Kinase MLK4 Determines Mesenchymal Identity in Glioma Stem Cells in an NF-κB-dependent Manner. Kim, S; Ezhilarasan, R; Phillips, E; Gallego-Perez, D; Sparks, A; Taylor, D; Ladner, K; Furuta, T; Sabit, H; Chhipa, R; et al. Cancer Cell. 2016; 29:201-213.

Selected

The AMPK inhibitor compound C is a potent AMPK-independent antiglioma agent. Liu, X; Chhipa, RR; Nakano, I; Dasgupta, B. Molecular Cancer Therapeutics. 2014; 13:596-605.

Selected

Discrete mechanisms of mTOR and cell cycle regulation by AMPK agonists independent of AMPK. Liu, X; Chhipa, RR; Pooya, S; Wortman, M; Yachyshin, S; Chow, LM L; Kumar, A; Zhou, X; Sun, Y; Quinn, B; et al. Proceedings of the National Academy of Sciences of the United States of America. 2014; 111:E435-E444.

Selected

Direct inhibition of retinoblastoma phosphorylation by nimbolide causes cell-cycle arrest and suppresses glioblastoma growth. Karkare, S; Chhipa, RR; Anderson, J; Liu, X; Henry, H; Gasilina, A; Nassar, N; Roychoudhury, J; Clark, JP; Kumar, A; et al. Clinical Cancer Research. 2014; 20:199-212.