KESS2 PhD in Biosciences: Delineating how oncogenic PI3K/PTEN signalling contributes to prostate cancer
|Application deadline||13 October 2017|
|Start date||1 January 2018|
|Level of study||Postgraduate research|
|Award type||PhD studentship|
|Number of studentships||1|
Prostate cancer (PCa) is the second major cause of cancer-related deaths in men, accounting for >300,000 deaths/annum worldwide.
Despite high response rates to androgen deprivation therapy (ADT) in advanced PCa patients, nearly all eventually develop progressive, castrate-resistant prostate cancer (CRPC). The mainstay of treatment for lethal CRPC is chemotherapy/ADT, yet survival is poor, emphasising the urgent clinical need to identify novel therapeutic strategies to treat PCa/CRPC.
Owing to the high frequency of oncogenic PI3K signalling in PCa/CRPC and its link to ADT resistance, this pathway is an attractive therapeutic target. Indeed loss of PTEN, a negative regulator of the PI3K pathway, occurs in 50-70% of PCa patients and is an inherent property of CRPC in mice.
Nevertheless, how the PI3K pathway contributes to PCa growth and CRPC transition is not clear. Dr. Pearson has recently discovered that hyperactivation of the PI3K catalytic subunit p110a (encoded by PIK3CA) causes rapid de novo castration resistance in combination with Pten loss, yet single mutants acquire CRPC over time.
This PhD project aims to establish the cooperating genetic events underpinning accelerated CRPC progression in Pik3ca-activated and Pten-deficient mutants, to develop a new ex-vivo platform for prostate cancer preclinical trials, and to identify/test novel therapeutic targets and diagnostic biomarkers.
This project offers a unique opportunity to delineate the molecular basis for CRPC in the context of Pten loss using a combination of clinically relevant transgenic models.
The PhD candidate will also develop a new panel of clinically relevant models to improve our molecular understanding of CRPC, and identify and rapidly test novel therapies. Ultimately, this work will provide critical insights into targeting the PI3K pathway in PCa patients, and has immediate implications for the design of clinical trials.
|Tuition fee support||Full UK/EU tuition fees|
|The KESS2 scholarship will provide a stipend, plus c. £3K a year available to support project-related expenses. Fees will be met by the University.|
|Maintenance stipend||Starting stipends of £14,198 per year for PhD studentships and £11,358 a year for MRes/MPhil studentships (exact figures subject to confirmation of start date and an income assessment).|
|Residency||UK Research Council eligibility conditions apply|
Applicants for research PhDs at Cardiff University are expected to have one or both of the following:
- have a home or work address in the West Wales and the Valleys region at the time of their application for KESS funding and their enrolment for the course of study
- have a legal right to live and work in the UK for the duration of the KESS2 support, and the right to take up paid work in the WWV region on completion of the scholarship
- be classified as a ‘home’ or ‘EU’ student.
The Convergence area covers West Wales and the Valleys, and is made up of the following 15 local authorities:
- Isle of Anglesey
- Neath Port Talbot
- Rhondda Cynon Taf
- Merthyr Tydfil
- Blaenau Gwent
Applicants must also be prepared to provide proof of identity and income as part of the stipend assessment process. Further details are available from the KESS2 Office.
Consideration is automatic upon application for admission to the Doctor of Philosophy in Biosciences with a January 2018 start date.
In the funding section of your application, please select 'I will be applying for a scholarship/grant' and specify that you are applying for advertised funding from KESS2. In the research proposal section, include the project description contained here.
We reserve the right to close applications early should sufficient applications be received.
Funding opportunity provided by: