91探花

Reetobrata Basu

Reetobrata Basu, portrait
Research Associate 1
Konneker 218

Department of Biomedical Sciences/Edison Biotechnology Institute, Heritage College of Osteopathic Medicine

Degrees earned:

Ph.D. in Molecular Cellular Biology/ August 2016/ 91探花/ Athens, Ohio, USA

M.S. in Neuroscience/ December 2014/ 91探花/ Athens, Ohio, USA

MSc in Biochemistry/ July 2007/ Bangalore University/ Bangalore, Karnataka, India

BSc in Chemistry/ July 2005/ Calcutta University (Presidency College)/ Kolkata, West Bengal, India

Research

In my research we aim to identify the mechanisms by which cancer cells develop resistance to available anti-cancer therapies, and how to re-sensitize them. Over the course of last five years, we have discovered a growth hormone (GH) regulated axis in driving drug efflux, phenotype switch, and drug sequestration in intracellular compartments in human melanoma. We have also found that drug-resistant human melanoma liver cancer, and pancreatic cancer can be re-sensitized to chemotherapy by a concomitant inhibition of the GH receptors (GHR) on these tumors. My research provides the mechanistic groundwork which upholds the translational approach to treat GH responsive human cancers with a combination of GHR antagonists and anti-cancer drugs. In addition, we are involved in multiple peptide-based collaborative drug-discovery projects.

Selected Publications

S. Duran-Ortiz, E. List, R. Basu, J. J. Kopchick. Extending lifespan by modulating the growth hormone / insulin like growth factor 1 axis: coming of age. Pituitary (2021) doi: 10.1007/s11102-020-01117-0 

Qian Y*, Basu R*, Arnett NA, Mathes SC, Duran-Ortiz S, Funk KR, Brittain AL, Singerman JT, Terry J, Henry BE, List EO, Berryman DE, & Kopchick JJ (* equal contribution). Growth hormone upregulates mediators of melanoma drug efflux and epithelial-to-mesenchymal transition in vitro and in vivo. Cancers (Basel) (2020) 12, 3640, doi: 10.3390/cancers12123640 

List, E. O., Basu, R., Duran-Ortiz, S., Krejsa, J. & Jensen, E. A. Mouse models of growth hormone deficiency. Rev. Endocr. Metab. Disord. (2020). doi:10.1007/s11154-020-09601-5 

E. O. List, D. E. Berryman, R. Basu, M. Buchman, K. Funk, P. Kulkarni, S. Duran-Ortiz, Y. Qian, E. A. Jensen, J. A. Young, G. Yildirim, S. Yakar, J. J. Kopchick, The Effects of 20-kDa Human Placental GH in Male and Female GH-deficient Mice: An Improved Human GH? Endocrinology. 161 (2020), doi:10.1210/endocr/bqaa097. 

S. Duran-Ortiz, J. Young, A. Jara, E. Jensen, R. Basu, E. O. List, D. E. Berryman, Differential gene signature in adipose tissue depots of growth hormone transgenic mice. Journal of Neuroendocrinology. (2020), doi: 10.1111/jne.12893 

Basu R, Kulkarni P, Qian Y, Walsh C, Arora P, Davis E, Duran-Ortiz S, Funk K, Ibarra D, Kruse C, Mathes S, McHugh T, Berryman DE, List EO, Okada S, Kopchick JJ. Growth hormone upregulates melanocyte inducing transcription factor (MITF) expression and activity via JAK2-STAT5 and SRC signaling in GH receptor (GHR)-positive human melanoma. Cancers (2019); doi: . 

Basu R & Kopchick JJ. The Effects of Growth Hormone on Therapy Resistance in Cancer. Cancer Drug Resistance (2019); doi: 10.20517/cdr.2019.27            

Basu R, Qian Y, & Kopchick JJ. Mechanisms in Endocrinology: Lessons from growth hormone receptor gene disrupted mice: Are there benefits of endocrine defects? European Journal of Endocrinology. (2018); doi:10.1530/EJE-18-0018. 

Basu R, Baumgaertel N, Wu S, Kopchick JJ. Growth Hormone Receptor Knockdown Sensitizes Human Melanoma Cells to Chemotherapy by Attenuating Expression of ABC Drug Efflux Pumps. Hormones and Cancer.(2017); doi:10.1007/s12672-017-0292-7 

Basu R, Wu S, Kopchick J. Targeting growth hormone receptor in human melanoma cells attenuates tumor progression and epithelial mesenchymal transition via suppression of multiple oncogenic pathways. Oncotarget, (2017); doi: 10.18632/oncotarget.15375. 

Brittain A, Basu R, Qian Y, Kopchick J. Growth Hormone and the Epithelial-to-Mesenchymal Transition. Journal of Clinical Endocrinology and Metabolism (2017); doi: .