ABSTRACT

Prostate cancer (PCa) is a common disease associated with high morbidity and mortality. Despite efforts to profile PCa on transcriptional and proteomic levels, the potential genetic alterations and underlying molecular biological signal pathways that may correlate with disease progression have not yet been resolved. Unfortunately, current clinical diagnostic, prognostic and predictive biomarkers can only partially explain the clinical outcomes which vary from patient to patient. The objective of this review is to investigate the TMPRSS2: ERG and other ETS-family gene fusions including heterogeneity in relation to their unique molecular biological features from localized PCa to systemic metastasis. Progress in personalized medicine has relied on rapid genomic analyses and expanding portfolio of targeting agents. In this respect, we will try to clarify how the molecular processes work and what might be the molecular targets in personalized treatment in metastatic castration resistant prostate cancer (mCRPC). Individually designed treatments- tailored therapy-could be developed, if the molecular basis of the disease is clarified through establishing correlations with variations among individuals. This may allow for significant improvements in survival rates and quality of life of affected individuals.