Prostate cancer (PCa) is the second most commonly diagnosed malignancy and has an extremely heterogeneous clinical behavior.
The vast majority of PCas are hormonally driven diseases in which androgen signalling plays a central role. The realization that castration resistant prostate cancer (CRPC) continues to rely on androgen signalling prompted the development of new, effective androgen blocking agents. As the understanding of the molecular biology of PCas evolves, it is hoped that stratification of prostate tumours into distinct molecular entities, each with its own set of vulnerabilities, will be a feasible goal. Around half of PCas harbour rearrangements involving a member of the ETS transcription factor family. Tumours without this rearrangement include SPOP mutant as well as SPINK1 overexpressing subtypes. As the number of targeted therapy agents increases, it is crucial to determine which patients will benefit from these interventions and molecular pathology will be key in this respect. In addition to directly targeting cells, therapies that modify the tumour microenvironment have also been successful in prolonging the life of PCa patients. Understanding the molecular aspects of PCa therapeutics will allow pathologists to provide core recommendations for patient management.
Written by:
Rodrigues DN, Butler LM, Estelles DL, de Bono JS. Are you the author?
Prostate Cancer Targeted Therapy Group and Drug Development Unit, The Royal Marsden NHS Foundation Trust and The Institute of Cancer Research, Downs Road, Sutton, Surrey, UK, SM2 5PT.
Reference: J Pathol. 2013 Sep 20. Epub ahead of print.
doi: 10.1002/path.4272
PubMed Abstract
PMID: 24108540
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