ORIGINAL ARTICLE
Year : 2014  |  Volume : 16  |  Issue : 6  |  Page : 829-832

Identification of speckle-type POZ protein somatic mutations in African American prostate cancer


1 Department of Biology, School of Science, Technology, Engineering, and Mathematics, Dillard University, New Orleans, LA, USA, New Orleans, LA, USA
2 Department of Genetics; Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA
3 Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA
4 Biospecimen Core Laboratory, Louisiana Cancer Research Consortium, New Orleans, LA, USA
5 Stanley S. Scott Cancer Center; Department of Pediatrics, Louisiana State University Health Sciences Center, New Orleans, LA, USA

Correspondence Address:
Wanguo Liu
Department of Genetics; Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1008-682X.132470

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The speckle-type POZ protein (SPOP) is a tumor suppressor in prostate cancer (PCa). SPOP somatic mutations have been reported in up to 15% of PCa of those of European descent. However, the genetic roles of SPOP in African American (AA)-PCa are currently unknown. We sequenced the SPOP gene to identify somatic mutations in 49 AA prostate tumors and identified three missense mutations (p.Y87C, p.F102S, and p.G111E) in five AA prostate tumors (10%) and one synonymous variant (p.I106I) in one tumor. Intriguingly, all of mutations and variants clustered in exon six, and all of the mutations altered conserved amino acids. Moreover, two mutations (p.F102S and p.G111E) have only been identified in AA-PCa to date. Quantitative real-time polymerase chain reaction analysis showed a lower level of SPOP expression in tumors carrying SPOP mutations than their matched normal prostate tissues. In addition, SPOP mutations and novel variants were detected in 5 of 27 aggressive PCa and one of 22 less aggressive PCa (P < 0.05). Further studies with increased sample size are needed to validate the clinicopathological significance of these SPOP mutations in AA-PCa.


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