Spotlight on the Laboratory of Dr. Nilesh Gaikwad
In humans many physiological processes are controlled by steroids, including reproduction, cardiovascular health and neurological functions. Although steroids play a broad and vital role in human physiology, they are also implicated in the development and/or progression of many diseases, such as breast cancer, ovarian cancer, prostate cancer, endometrial cancer, liver cancer, colon cancer, osteoporosis, neurodegenerative diseases, cardiovascular disease and obesity.
Present evidence shows the involvement of many steroids such as estrogens, testosterone, bile acids, oxysterols, etc. in carcinogenic processes. Gathering evidence suggests that oxidative metabolism of steroids can cause cancer, neurodegenerative and other diseases. Given this, the overall objective of research in the Gaikwad Lab is to develop tandem mass spectrometry based metabolomics platform and explore various steroid metabolic pathways in humans. The lab is also exploring steroid metabolic signatures in various models to develop biomarkers for early detection of cancers, neurological diseases and to study disease mechanisms. In addition, one of the major goals of the Gaikwad Lab is to study diet/food component(s) which alter the course of steroid metabolic pathways that are responsible for diseases. Gaikwad lab researchers are also interested in elucidating mechanisms of action of toxins that can alter steroid metabolic pathways.
Recent publications by lab members include:
- Guo Y, Hu B, Huang Y, Tsung A, Gaikwad N, Xu M, Jiang M, Ren S, Fan J, Billiar TR, Huang M, and Xie W. Estrogen sulfotransferase is an oxidative stress responsive gene that gender-specifically affects liver ischemia/reperfusion injury, Journal of Biological Chemistry, doi:10.1074/jbc.M115.642124, 2015. [PubMed]
- Chengfei Liu, Wei Lou, Yezi Zhu, Joy C. Yang, Nagalakshmi Nadiminty, Nilesh W.Gaikwad, Christopher P. Evans, Allen C. Gao. Intracrine androgens and AKR1C3 activation confer resistance to enzalutamide in prostate cancer, Cancer Research, 75, 1413-1422, 2015. [PubMed]
- Hemantkumar Chavan, Feng Li, Robert Tessman, Kristine Mickey, Kenneth Dorko, Timothy Schmitt, Sean Kumer, Sumedha, Gunewardena, Nilesh Gaikwad, and Partha Krishnamurthy. Metabolic disturbance in the ATP binding cassette transporter Abcb6 deficient mice results in suppression of hepatic Cytochrome P450 activity, Journal of Biological Chemistry, 290: 7871-7886, 2015. [PubMed]