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Sequencing the genes of 112 prostate cancers found the disease's commonest point mutation in a gene nobody had linked to it, and showed those tumours are a separate kind that never carries the usual fusion.
The exomes of 112 prostate tumour and normal tissue pairs were sequenced. New recurrent mutations were identified in multiple genes including MED12 and FOXA1. SPOP was the most frequently mutated gene, with mutations involving the SPOP substrate-binding cleft in 6 to 15% of tumours across multiple independent cohorts. Prostate cancers with mutant SPOP lacked ETS family gene rearrangements and showed a distinct pattern of genomic alterations, so SPOP mutation appears to define a molecular subtype.
It established the fusion-negative side of the prostate cancer taxonomy and made SPOP the disease's signature point mutation, in a ubiquitin ligase adaptor rather than in a kinase, which is part of why prostate cancer has so few druggable drivers.
Shares FOXA1, SPOP, Somatic mutations from exome and genome sequencing (WXS, WGS), ERG.
Shares FOXA1, SPOP, SPOP mutation, Somatic mutations from exome and genome sequencing (WXS, WGS).
Shares ERG, Prostate cancer (KEGG map), Androgen receptor signalling, Gene fusion.
Shares FOXA1, Somatic mutations from exome and genome sequencing (WXS, WGS), ERG, Prostate cancer (KEGG map).
Shares SPOP mutation, ERG, Prostate cancer (KEGG map), Androgen receptor signalling.
Shares FOXA1, Prostate cancer (KEGG map), Androgen receptor signalling, Driver mutation.
Shares ERG, Prostate cancer (KEGG map), Androgen receptor signalling, Gene fusion.
Shares SPOP, SPOP mutation, Androgen receptor signalling, Driver mutation.