Doctor of Philosophy [Ph.D] (KESS2 PhD in Biosciences: Delineating how oncogenic PI3K/PTEN signalling contributes to prostate cancer)
3 years
Full Time
Important Dates
University allocates places on a first-come, first-served basis, so students are recommended to apply as early as possible.
- 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.
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