Molecular mechanisms driving prostate cancer neuroendocrine differentiation
  Prostate cancer is the second most common cancer amongst males and 10,000 deaths per year are attributed to the disease in the United Kingdom alone. On average, prostate cancer tumours become resistant to androgen deprivation therapy within two years. These resistant tumours are markedly more aggressive and likely to metastasise, after which the disease is considered incurable. The research objective is to analyse the changes that occur within prostate cancer cells as they become resistant and to identify key genes and proteins which may be suitable therapeutic targets. Specifically, the project has identified that prostate cancer cells differentiate into a neuronal-like state in response to androgen deprivation therapy. This hybrid phenotype appears to confer prostate cancer cells with treatment resistance, increased ability of disease recurrence and paracrine tumour support potential. Work is currently focused upon assessing the viability of multiple genes and proteins in the neuronal differentiation process as treatment targets and studying how these changes can be prevented or reversed. Ultimately, the project has potential to inform clinically on the use of optimised androgen deprivation strategies to delay onset of resistance. The research will also be of interest to both prostate cancer researchers and the wider cancer research community, where neuronal differentiation has been implicated in multiple cancer types yet its specific roles remain largely unelucidated.

  • Dates:

    2014 to 2019

  • Qualification:

    Doctorate (PhD)

Project Team