INVITED RESEARCH HIGHLIGHT
Year : 2014  |  Volume : 16  |  Issue : 5  |  Page : 659-660

Speckle-type POZ protein mutations interrupt tumor suppressor function of speckle-type POZ protein in prostate cancer by affecting androgen receptor degradation


Cancer Program, Institute of Health and Biomedical Innovation; Australian Prostate Cancer Research Centre-Queensland, Translational Research Institute, Queensland University of Technology, Brisbane, Queensland, Australia

Correspondence Address:
Jyotsna Batra
Cancer Program, Institute of Health and Biomedical Innovation; Australian Prostate Cancer Research Centre-Queensland, Translational Research Institute, Queensland University of Technology, Brisbane, Queensland
Australia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1008-682X.133323

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Large scale exome sequencing studies have revealed regions of the genome, which contribute to the castrate resistant prostate cancer (CRPC) phenotype. [1],[2],[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, particularly in the context of SPOP-mediated degradation of the AR.


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