Vikram Bhatia
Postdoctoral Fellow
Biochemistry & Medical Genetics
Canada
Biography
Dr. Vikram Bhatia is presently working as post doctoral fellow in the Department of Biochemistry and Medical Genetics, University of Manitoba from March 2016 till present. He received his M.Sc. (2006) from Chhatrapati Shahu Ji Maharaj University, Kanpur, India, and B.Sc. (2004) from University of Lucknow, U.P., India. Dr. Bhatia received his Ph.D. degree from the King George’s Medical University, Lucknow, India in 2016. His thesis work was entitled as “Promoter DNA Hypermethylation of Critical Genes and MicroRNA Levels in Oral Cancer and Precancerous Lesions”. During Ph.D. he got Indian Council of Medical Research - Senior Research Fellowship and afterwards, he worked as a Scientist-B in Indian Council of Medical Research funded project entitled: “Epigenetic alterations associated with mesenchymal transition in endometrial intraepithelial neoplasia and endometrioid endometrial carcinoma” in the Department of Pathology, King George's Medical University, Lucknow, India.
Research Interest
Role of ubiquitin carboxyl-terminal hydrolase isoenzyme 1 (UCHL1) in genome organization. UCHL1 is a member of the peptidase C12 family and has both the enzymatic activity to remove or add ubiquitin to proteins. Removal of ubiquitin is done through the enzyme's thiol protease activity, which hydrolyzes the peptide bond at C-terminal glycine of ubiquitin. UCHL1 expression is correlated with poor prognosis in many cancer types. The literature depicts UCHL1 as an oncogene (breast cancer) and a tumor suppressor gene (prostate cancer). It has multiple functions including maintaining ubiquitin homeostasis, protein degradation and regulating cyclin-dependent kinase activity. The primary objective of the study is to see the role of UCHL1 in regulating the genome organization and function of the cancer cell genome.
Publications
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Chandra S, Goel MM, Makker A, Nayak S, Shilpi P, Bhatia V, Bhatt MLB. Lymphangiogenesis in oral squamous cell carcinoma and potentially malignant oral lesions. Int J Pharm Bio Sci 2014 Jan; 5(1): (B) 983 - 993.
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Bhatia V, Goel MM, Makker A. DNA Methylation: An Epigenetic Mechanism in Oral Squamous Cell Carcinoma. South Asian Journal of Environmental Biology 2014; 4 (2): 33-41.
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Nayak S, Goel MM, Makker A, Bhatia V, Chandra S, Kumar S, Agarwal SP. Fibroblast Growth Factor (FGF-2) and its Receptors FGFR-2 and FGFR-3 may be Putative Biomarkers of Malignant Transformation of Potentially Malignant Oral Lesions into Oral Squamous Cell Carcinoma. PlosOne; October 14, 2015