Dr. Khalid Zaffar Masoodi was born at Narwara near Iddgah in Srinagar, J&K, India in April 1979. His father was a renowned doctor and educator.
Education
From the age of 3 to 15 Khalid Z. Masoodi went to Burn Hall School, Srinagar. In 1996 Masoodi went to Aligarh Muslim University where he obtained his +2 and BSc (Botany Hons) in 2002.
In 2002 Department of Biotechnology, Govt. of India selected Khalid Z. Masoodi for Merit Scholarship to pursue MSc in biotechnology from Jammu University through National level exam where he derived the mechanism of gene amplification in Plantago lagopus (Mediterranean Plantain ). In 2006 after qualifying, CSIR-NET and GATE and securing 25th all India rank in DBT-BET-JRF He joined PhD under the supervision of Prof. Manoj K. Dhar a renowned Cytogeneticist and Biotechnologist of India. He discovered two new genes from Purple Black carrot and reconstructed carrot carotenoid biosynthetic pathways in E. coli using Gene Amplification technology (GAT) and completed his PhD in Plant Biotechnology in 2010.
Career
For his work on GAT he was offered a position as a Postdoc in Prof. Zhou Wang's Lab, University of Pittsburgh, Pennsylvania, USA from June 2010 till May 2014 where he worked on Drug Discovery and Gene Discovery against Prostate Cancer. At University of Pittsburgh he worked on multiple projects simultaneously being an expert in Biotechnology-an interdisciplinary subject. In Dec 2014 Khalid Z. Masoodi joined as assistant professor of Plant Biotechnology at SKUAST-Kashmir, Shalimar, J&K, India. He published his first scientific paper in 2013 (.) where he used animal model to increase the efficacy of Intermittent Androgen deprivation therapy for prostate cancer patients.
From 2010 to 2015 The focus of his research was extensively on 3 aspects of Drug discovery and gene discovery against Prostate cancer. Modifying old therapies for Prostate cancer Drug discovery for treating Prostate cancer using small molecule inhibitors (nanoparticles) Gene discovery for prostate cancer that can act as new targets for different therapies. i. Androgen deprivation therapy (ADT) is the standard treatment for patients with prostate-specific antigen progression after treatment for localized prostate cancer. An alternative to continuous ADT is intermittent ADT (IADT), which allows recovery of testosterone during off-cycles to stimulate regrowth and differentiation of the regressed prostate tumor. His findings suggest that short off-cycle coupled with 5ɑ-reductase inhibition could maximize suppression of prostate tumor growth and, thus improve potential survival benefit achieved in combination with IADT. He found out that the efficacy of IADT can be improved by finasteride or dutasteride administration when short fixed off-cycle intervals are used. Further extrapolating this study in mice he found out that 5α-reductase inhibition in shorter off-cycles of testosterone recovery could maximize tumor growth inhibition during IADT and perhaps increase survival. This finding can be used to help design future clinical trials testing whether 5ARI coupled with short off-cycles can prolong the survival of prostate cancer patients on IADT. For his work Dr. Khalid Masoodi was conferred with Travel Award by the Society of Basic Urology Research (SBUR, USA) for the SBUR 2012 SBUR Fall Symposium held on 15–18 November 2012 at the Trump International Beach Resort in Miami, Florida, USA. ii.
Dr. Khalid Z. Masoodi helped in discovering the role of Four major genes that have a role in prostate cancer progression. The data suggested that DHX15 enhances AR transcriptional activity and contributes to PCa progression through Siah2 mediated ubiquitination of androgen receptor. Another gene Prp8 was shown to be a novel AR cofactor that interacts with NES(AR) and regulates AR function in prostate cancer cells. The study suggested that PABPC1 another candidate is an important AR co-regulator capable of promoting AR nuclear localization and function via interaction with the NTD region. Elevated expression of PABPC1 in prostate cancer specimens is likely to play an important role in prostate carcinogenesis by enhancing AR signalling pathways. Elongation factor, RNA polymerase II, 2 (ELL2) and its pathway genes were shown to play an important role in the development and progression of prostate cancer. For this finding he was conferred with Journal Award for publishing best paper in Endocrinology by Society of Endocrinology, Glasgow, United Kingdom on 19 Nov 2018. iii.