摘要
Large scale exome sequencing studies have ＇revealed regions of the genome, which contribute to the castrate resistant prostate cancer （CRPC） phenotype.1-3 Such studies have identified mutations in genes, which may have diagnostic/prognostic potential, or which may be targeted therapeutically. Two of these genes include the androgen receptor （AR） and speckle-type POZ protein （SPOP） genes. However, the findings from these exome sequencing studies can only be translated therapeutically once the functional consequences of these mutations have been determined. Here, we highlight the recent study by An et al.4 which investigated the functional effects of mutations in the SPOP gene that were identified in the aforementioned exome sequencing studies, particnlarly in the context of SPOP-mediated degradation of the AR.
Large scale exome sequencing studies have ＇revealed regions of the genome, which contribute to the castrate resistant prostate cancer （CRPC） phenotype.1-3 Such studies have identified mutations in genes, which may have diagnostic/prognostic potential, or which may be targeted therapeutically. Two of these genes include the androgen receptor （AR） and speckle-type POZ protein （SPOP） genes. However, the findings from these exome sequencing studies can only be translated therapeutically once the functional consequences of these mutations have been determined. Here, we highlight the recent study by An et al.4 which investigated the functional effects of mutations in the SPOP gene that were identified in the aforementioned exome sequencing studies, particnlarly in the context of SPOP-mediated degradation of the AR.
