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dc.contributor.authorGrisanzio, Chiara
dc.contributor.authorWerner, Lillian
dc.contributor.authorTakeda, David
dc.contributor.authorAwoyemi, Bisola C.
dc.contributor.authorPomerantz, Mark M.
dc.contributor.authorYamada, Hiroki
dc.contributor.authorSooriakumaran, Prasanna
dc.contributor.authorRobinson, Brian D.
dc.contributor.authorLeung, Robert
dc.contributor.authorSchinzel, Anna C.
dc.contributor.authorMills, Ian
dc.contributor.authorRoss-Adams, Helen
dc.contributor.authorNeal, David E.
dc.contributor.authorKido, Masahito
dc.contributor.authorYamamoto, Toshihiro
dc.contributor.authorPetrozziello, Gillian
dc.contributor.authorStack, Edward C.
dc.contributor.authorLis, Rosina
dc.contributor.authorKantoff, Philip W.
dc.contributor.authorLoda, Massimo
dc.contributor.authorSartor, Oliver
dc.contributor.authorEgawa, Shin
dc.contributor.authorTewari, Ashutosh K.
dc.contributor.authorHahn, William C.
dc.contributor.authorFreedman, Matthew L.
dc.date.accessioned2019-10-13T16:02:53Z
dc.date.issued2012
dc.identifier.citationGrisanzio, C., L. Werner, D. Takeda, B. C. Awoyemi, M. M. Pomerantz, H. Yamada, P. Sooriakumaran, et al. 2012. “Genetic and Functional Analyses Implicate the NUDT11, HNF1B, and SLC22A3 Genes in Prostate Cancer Pathogenesis.” Proceedings of the National Academy of Sciences 109 (28): 11252–57. doi:10.1073/pnas.1200853109.
dc.identifier.issn0027-8424
dc.identifier.issn0744-2831
dc.identifier.issn1091-6490
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41542762*
dc.description.abstractOne of the central goals of human genetics is to discover the genes and pathways driving human traits. To date, most of the common risk alleles discovered through genome-wide association studies (GWAS) map to nonprotein-coding regions. Because of our relatively poorer understanding of this part of the genome, the functional consequences of trait-associated variants pose a considerable challenge. To identify the genes through which risk loci act, we hypothesized that the risk variants are regulatory elements. For each of 12 known risk polymorphisms, we evaluated the correlation between risk allele status and transcript abundance for all annotated protein-coding transcripts within a 1-Mb interval. A total of 103 transcripts were evaluated in 662 prostate tissue samples [normal (n = 407) and tumor (n = 255)] from 483 individuals [European Americans (n = 233), Japanese (n = 127), and African Americans (n = 123)]. In a pooled analysis, 4 of the 12 risk variants were strongly associated with five transcripts (NUDT11, MSMB, NCOA4, SLC22A3, and HNF1B) in histologically normal tissue (P <= 0.001). Although associations were also observed in tumor tissue, they tended to be more attenuated. Previously, we showed that MSMB and NCOA4 participate in prostate cancer pathogenesis. Suppressing the expression of NUDT11, SLC22A3, and HNF1B influences cellular phenotypes associated with tumor-related properties in prostate cancer cells. Taken together, the data suggest that these transcripts contribute to prostate cancer pathogenesis.
dc.language.isoen_US
dc.publisherNational Academy of Sciences
dash.licenseLAA
dc.titleGenetic and functional analyses implicate the NUDT11, HNF1B, and SLC22A3 genes in prostate cancer pathogenesis
dc.typeJournal Article
dc.description.versionVersion of Record
dc.relation.journalProceedings of the National Academy of Sciences of the United States of America
dash.depositing.authorHahn, William C::31ef101c797e643e0dfa48f8bce1dc3c::600
dc.date.available2019-10-13T16:02:53Z
dash.workflow.comments1Science Serial ID 87059
dc.identifier.doi10.1073/pnas.1200853109
dash.source.volume109;28
dash.source.page11252


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