Consistent with our findings, studies have demonstrated that RAD51 expression and foci formation remain unchanged in other PTEN-deficient tumor cell lines (isogenic HCT116/PTEN−/−, PC-3, and U251MG), primary astrocytes, RNAi studies (shPTEN-expressing H1299), comparative prostatic tumor xenograft analyses (PTEN+/+ 22RV1; PTEN+/− DU145; and PTEN−/− PC3), and human tumor tissue microarrays [29,34,35,76]. This evidence concerns the gene RAD51 and neoplasm.