Figure 5.

Proposed etiology of DNA damage in the “referred” prostate biopsies and prostate cancer risk. In response to DNA damage in the prostate, cellular and systemic tumor surveillance pathways could be initiated to prevent tumorigenesis or cancer development. Protection at cellular level is through activation of ATM to initiate DNA repair or apoptosis of damaged cells. Protection at systemic level is through the induction of MIC expression to alert of NK cell-mediated innate immunity. In the incidence of accumulation of mutations in DNA repair or apoptosis pathways, genomic instability will occur and lead to prostate tumorigenesis. Compromised NK cell function will enable tumor immune evasion and facilitate cancer development.