Dr. Mohammad Asim is a cancer biologist and a university lecturer (Assistant Professor) who graduated with a first class Bachelor's in Science, and then a Masters in Science degree from Hamdard University, New Delhi, India. He was awarded a PhD degree by the Justus Liebig University in Germany for his work uncovering the role of signal transduction pathways and transcriptional corepressors in the regulation of Androgen Receptor (AR) signalling in prostate cancer (PCa). His PhD work identified LCoR as a novel transcriptional corepressor for the AR and uncovered its cross-talk with Src kinase pathway. In 2007, he embarked on his first postdoctoral training in Cancer Biology at the University of Wisconsin, Madison, USA where he identified novel small molecules with potential to inhibit AR signalling in PCa. In 2010 he took up a senior postdoctoral position at the CR UK institute of the University of Cambridge, UK. After spending more than 6 years at Cambridge, in 2016 he was appointed as a full-time university lecturer at the University of Surrey.

Mohammad has over a decade experience on researching the molecular mechanisms that lead to prostate cancer progression. His research has focussed on understanding the role of AR in PCa and has been proven vital in finding novel treatment for aggressive PCa.

Lethal prostate cancer: Finding it early and identifying effective treatments

Mohammad has keen interest and research expertise in the area of Prostate cancer (PCa). PCa is a leading cause of cancer related mortality in the United Kingdom with 11,000 deaths each year. There are a number of hurdles in the successful clinical management of the disease. On one side of the spectrum, Prostate-specific antigen (PSA) screening does reduce the risk of dying of PCa by 20%, however there are a number of cases of overdiagnosis and overtreatment inherent in PCa screening which is fairly non-specific. Therefore, to identify which patients must receive treatment and which patients should be monitored by “watchful waiting” is a clinical challenge. On the other side of the spectrum, why standard hormone therapy fails and how cancer becomes aggressive is poorly understood and leaves PCa patients with limited treatment options.

Dr. Asim’s strongly believes that a multi-dimension interdisciplinary research to attack PCa from different angles holds the key for the development of successful therapies with sustained clinical benefits. In terms of early detection, understanding underlying biology behind early disease could pave the way towards development of more specific diagnostic tools and will be vital in PCa patient survival, to avoid unnecessary overtreatment for those who do not need it and to decrease financial burden on health services. Moreover, understanding mechanisms that allow the disease to progress and become aggressive is vital in identifying novel therapeutic targets and thus important in designing novel therapies to treat PCa. Mohammad’s current research projects include:

1. Understanding the onset of PCa to develop precision diagnostic tools. 2. To understand the function of AR in the end-of-spectrum disease. 3. Identification and validation of novel potential drug targets in PCa. 4. Designing novel strategies to block PCa progression.

Asim M, Massie CE, Neal DE. (2016) ‘Kinase joins the chaperone club: Androgen-regulated kinome reveals choline kinase alpha as a potential drug target in prostate cancer.’ Mol Cell Oncol. 2016 Feb 24;3(3):e1140262. Asim M$, Massie CE, Orafidiya F, Pértega-Gomes N, Warren AY, Selth LA, Zecchini HI, Qureshi A, Baridi A, Menon S, Madhu B, Escriu C, Lyons S, Zecchini V, Shaw G, Hessenkemper W, Russell R, Mohammed H, Stefanos N, Lynch AG, Grigorenko E, D’Santos C, Taylor C, Lamb A, Sriranjan R, Yang J, Stark R, Dehm SM, Rennie PS, Baniahmad A, Carroll JS, Griffiths JR, Tavaré S, McEwan IJ, Mills IG, Tilley WD, & Neal DE. (2015) ‘Choline kinase alpha is an Androgen Receptor Chaperone and Prostate Cancer Therapeutic Target’ J Natl Cancer Inst. 2015 Dec 11;108(5). ($Joint first and corresponding author) Asim M, Hafeez BB, Siddiqui IA, Gerlach C, Patz M, Mukhtar H, Baniahmad A. (2011) ‘Ligand-dependent corepressor acts as a novel androgen receptor corepressor, inhibits prostate cancer growth, and is functionally inactivated by the Src protein kinase.’ Journal of Biological Chemistry Oct 28;286(43):37108-17. Siddiqui IA, Asim M$, Hafeez BB, Adhami VM, Tarapore RS, Mukhtar H. (2011) ‘Green tea polyphenol EGCG blunts androgen receptor function in prostate cancer.’ FASEB Journal Apr;25(4):1198-207 ($Joint first author) Eisold M, Asim M, Eskelinen H, Linke T, Baniahmad A. (2009) ‘Inhibition of MAPK-signaling pathway promotes the interaction of the corepressor SMRT with the human androgen receptor and mediates repression of prostate cancer cell growth in the presence of antiandrogens.’ J Mol Endocrinol. May;42(5):429-35.