“…For prostate cancer, the most intensively investigated associations have related to genes in the following pathways: adhesion molecules (CDH1); androgen metabolism (AR, ESR2, SRDA2,); angiogenesis (VEGF) angiotensin conversion (ACE); baseexcision repair (XRCC1); inflammation and immune response (IL8, IL10, MSR1, PTGS2, TNF); inhibition of cell growth (FGFR4, TGFB1, TGFBR1); insulin-like growth factor metabolism (IGF1, IGFBP3); one carbon metabolism (MTHFR, diverse genes139); oxidative response (MnSOD, hOGG1); substrate metabolism (CYP1A1, CYP3A4, CYP17, GSTM1, GSTT1, GSTP1, NAT1 and NAT2, UGT2B17); vitamin D metabolism (VDR); and, common variants of genes for which rare mutations are associated with increased cancer risk (ELAC/HPC2, RNASEL, TP53, MDM2,) [36][37][38][39][40][41][42][43][44][45][46][47][48][49][50]. In general, the results of candidate gene studies have been inconclusive, for reasons discussed in many interpretations [51,52].…”