Understanding the molecular mechanisms that drive castration resistant prostate cancer

Prostate cancer is a leading cause of cancer related deaths in the United Kingdom. This is due to cancer developing resistance to standard of care therapy known as androgen deprivation therapy. The key question this project will address is why does the ADT fail and how can we circumvent this problem to develop curative treatment for prostate cancer.

Start date
1 October 2019
3 years
Application deadline
Funding source
Prostate Cancer Foundation
Funding information

PI will cover the cost towards Stipend, approximately £15K, and tuition fee for UK/EU students. International students are accepted provided they can cover the difference of Tuition fee between home and International students. Materials and consumables will be provided.


Prostate cancer (PrCa) is a leading cause of cancer related male mortality in the United Kingdom with over 11,000 deaths each year.

The growth and progression of PrCa is regulated by androgens, which manifest their action by activating the androgen receptor (AR), a ligand activated transcription factor that in turn regulates the growth of PrCa. Since AR signaling is upregulated in PrCa, it is an attractive drug target in the treatment of the advanced PrCa. Hence, widely used androgen deprivation therapy (ADT) is the mainstay treatment for PrCa, which is achieved by the use of anti-androgenic drugs such as Bicalutamide and Enzalutamide. ADT is initially effective but relapse is common leading to castration resistant prostate cancer (CRPC) for which there are no curative treatments. The key question is why does ADT fail and how can we develop more effective anti-androgens to target the AR?

This project will discover novel molecular mechanisms which can guide curative treatment for CRPC. Thus, the findings of this study will pave the way to effectively treat CRPC in order to alleviate the disease burden.

Eligibility criteria

You must have, or expect to achieve, at least a 2:1 honours degree or international equivalent in a relevant area of Biological Sciences.

You must have IELTS 7 with at least 6.5 in all the components.

Candidates should have good experience in cell culture and molecular biology techniques; some research experience working in a cancer research lab is highly desirable.

How to apply

Please email Mohammad Asim to discuss the project and for advice on completing the studentship form before applying through the Biosciences and Medicine PhD course page.

Biosciences and Medicine PhD

Application deadline

Contact details

Mohammad Asim
E-mail: m.asim@surrey.ac.uk

Department of clinical and experimental medicine

Molecular cancer biology


1. Anne Y. Warren, Charlie E. Massie, ---- David E. Neal and Mohammad Asim$ (2018) A reciprocal feedback between the PDZ binding kinase and androgen receptor in prostate cancer. Oncogene 2018 Sep 20. doi: 10.1038/s41388-018-0501-z. [Epub ahead of print].

2. Asim M, Tarish F, ---Neal DE and Helleday T (2017) Synthetic Lethality between androgen signaling and PARP pathway in Prostate Cancer. Nat Commun. Aug 29;8(1):374.

3. Asim M, Massie CE & Neal DE (2016) Kinase Joins the Chaperone Club: Androgen-Regulated Kinome Reveals Choline Kinase Alpha as Potential Drug Target in Prostate Cancer. Molecular & Cellular Oncology Feb 24;3(3):e1140262.

4. Asim M, Massie CE, ---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).


Studentships at Surrey

We have a wide range of studentship opportunities available.