For instance, cytogenetic studies based on fluorescence in situ hybridization have been used to describe the variability between CTCs, tumor metastasis and primary prostatic cancers in copy-number aberrations for the androgen receptor and presence of TMPRSS2-ERG fusions and loss of the tumor suppressor gene PTEN (encoding phosphatase and tensin homolog) [39]. This evidence concerns the gene AR and Familial prostate cancer.