Thomas A. White

TL;DR: SPOP mutations may define a new molecular subtype of prostate cancer, with mutations involving the SPOP substrate-binding cleft in 6–15% of tumors across multiple independent cohorts.

TL;DR: Analysis of multiple tumors from men with disseminated prostate cancer indicates that evaluating a single metastasis provides a reasonable assessment of the major oncogenic driver alterations that are present in disseminated tumors within an individual, and thus may be useful for selecting treatments on the basis of predicted molecular vulnerabilities.

TL;DR: The results indicate that point mutations arising in coding regions of advanced prostate cancers are common but, with notable exceptions, very few genes are mutated in a substantial fraction of tumors, and suggest that increasingly deep catalogs of human germline variation may challenge the necessity of sequencing matched tumor-normal pairs.

TL;DR: The National Human Genome Research Institute (U.S.) (Large Scale Sequencing Program Grant U54 HG003067) as discussed by the authors has provided a grant for large scale sequencing.

TL;DR: Amine catabolism by monoamine oxidase A contributes to oxidative stress, which plays a role in prostate cancer (PCa) development and progression, and may thereby affect PCa susceptibility.