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  Translational interrogations of prostate cancer


   Faculty of Health & Medical Sciences

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  Dr M Asim, Prof H Pandha  No more applications being accepted  Competition Funded PhD Project (European/UK Students Only)

About the Project

Applications are invited for a 3-year, fully-funded PhD studentship in the Targeted Cancer Therapy Group, Department of Clinical & Experimental Medicine, University of Surrey, Guildford. The department is headed by Prof. Simon de Lusignan and is home to the Surrey clinical research centre. This PhD position starts in April/May 2017 and is based primarily in the laboratory of Dr Mohammad Asim and will be jointly co-supervised by Prof. Hardev Pandha. Dr Asim has recently joined the department as a University lecturer and is a new group leader. He brings vast research experience on prostate cancer therapeutics having spent more than 6 years at the CR UK Cambridge Institute in the University of Cambridge (see references below for more information or visit http://www.surrey.ac.uk/biomed/people/mohammad_asim/ ).

The focus of this project is to understand the development of castration resistant prostate cancer (CRPC), which is an aggressive form of the disease with very limited treatment options. Understanding molecular mechanisms of CRPC and the key players in the resistance pathways to androgen deprivation therapy can be instrumental in predicting clinical behaviour of the disease and can have profound clinical benefits.

More specifically, this project will focus on interrogating the function of the androgen receptor (AR), which is master transcription factor regulating the growth and progression of prostate cancer.

The project will employ novel cellular and tissue based models to study prostate cancer with an overall aim to develop better therapeutics to treat CRPC. The department is active in clinical trials in men with advanced prostate cancer, and has access to fresh and archival prostate cancer tissue to add translational relevance to the PhD studentship.

As a PhD student you will work as part of vibrant and supportive research community and will receive extensive training for a career as a Cancer biologist.

Applicants should have:

1. At least an upper, second class honours degree (2.1) or equivalent in (but not restricted to) Biological/Biochemical sciences from a UK university or equivalent standard from an overseas University. Applications are particularly welcome from applicants who have a computation biology/bioinformatics degree with a keen desire to learn and apply their skills in wet-lab settings.

2. Fluency in English language.

3. Motivation and enthusiasm for work and should be capable of thinking and working independently.

4. British residency or EU nationality. The Faculty has a number of fully-funded PhD studentships for UK and EU nationals who can demonstrate the appropriate residency requirements. These studentships will include the tuition fees and a tax-free stipend. The Department has also a few scholarships for partial funding for overseas fees. However, funding for overseas students is limited and overseas students are encouraged to find suitable funding themselves.

The university values diversity and is committed to equality of opportunity.

Applications must quote the reference and include a cover letter, CV and at least contact details of two academic references. They must apply via the link on the apply online button below and then through the apply now button, while informal enquiries can be directed to [Email Address Removed]




Funding Notes

3-year fully funded PhD studentship

References

References:

(1) Kinase joins the chaperone club: Androgen-regulated kinome reveals choline kinase alpha as a potential drug target in prostate cancer. Asim M, Massie CE, Neal DE. Mol Cell Oncol. 2016 Feb 24;3(3).

(2) Choline Kinase Alpha as an Androgen Receptor Chaperone and Prostate Cancer Therapeutic Target. Asim M, Massie CE, (………) Neal DE. J Natl Cancer Inst. 2015 Dec 11;108(5).

(3) Ligand-dependent corepressor acts as a novel androgen receptor corepressor, inhibits prostate cancer growth, and is functionally inactivated by the Src protein kinase. Asim M, Hafeez BB, Siddiqui IA, Gerlach C, Patz M, Mukhtar H, Baniahmad A. J Biol Chem. 2011 Oct 28;286(43):37108-17.

(4) Src kinase potentiates androgen receptor transactivation function and invasion of androgen-independent prostate cancer C4-2 cells. Asim M, Siddiqui IA, Hafeez BB, Baniahmad A, Mukhtar H. Oncogene. 2008 Jun 5;27(25):3596-604.