Molecular pathology of prostate cancer: a practical approach

While localised prostate cancer can be cured by local treatment, ‘high-risk’ often progresses to castration resistant disease and remains incurable with a dismal prognosis. In recent years, technical advances development of novel methodologies have largely contributed better understanding underlying molecular mechanisms that promote tumour growth progression. Consecutively, therapeutic strategies for treatment emerged during the last decade, calling identification predictive biomarkers. The concept personalised medicine is tailor according specific profile an individual patient. Moreover, acquired changes evolution in response therapy selection pressure require adapted marker testing at different time points disease. this setting, pathologist plays critical role patient management selection.In review, we provide comprehensive overview current knowledge aspects their potential utility context approaches. Furthermore, discuss methods routine clinical practice, focus on cancer. selection. Prostate clinically biologically heterogeneous disease, which requires depending setting. patients newly diagnosed cancer, decisions radical or active surveillance depend tumour-related factors such as extent biopsies, histological subtype, Gleason/International Society Urological Pathology (ISUP) grade, serum antigen (PSA) level. However, order prevent overtreatment, there need additional prognostic markers more accurately predict biological behaviour support decision making. Apart from above mentioned factors, Gleason/ISUP grading being most powerful predictor outcome, particularly PTEN combination ERG, proliferation index Ki-67, are emerging value. On other hand, who initially present locally advanced metastatic show variable duration usually suffer several relapses sensitive eventually stage. As androgen receptor (AR) signalling pathway major progression, systemic primarily based antiandrogen (androgen deprivation therapy, ADT), optionally combined taxane-based chemotherapy. Through progress methodologies, gained new insights into resistance. Identification targets involving recurrently altered DNA repair phosphoinositide 3-kinase (PI3K)–AKT–mTOR has expanded landscape (CRPC). Notably, recognition reactivation AR CRPC led potent AR-targeted drugs second-generation antiandrogens abiraterone enzalutamide. still lack consensus optimal sequence use combinational strategies.1Gillessen S. Attard G. Beer T.M. et al.Management cancer: report conference 2019.Eur Urol. 2020; 77: 508-547Abstract Full Text PDF PubMed Scopus (164) Google Scholar Therefore, ongoing efforts establish biomarker various options identify possible primary secondary resistance mechanisms. By tailoring pathologists play key part contribute optimisation. 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