Markt, SarahRider, JenniferPenney, KathrynSchumacher, FredrickEpstein, MaraFall, KatjaSesso, HowardStampfer, MeirMucci, Lorelei2019-09-052014Markt, Sarah C., Jennifer R. Rider, Kathryn L. Penney, Fredrick R. Schumacher, Mara M. Epstein, Katja Fall, Howard D. Sesso, Meir J. Stampfer, and Lorelei A. Mucci. 2014. “Genetic Variation across C-Reactive Protein and Risk of Prostate Cancer.” The Prostate 74 (10): 1034–42. https://doi.org/10.1002/pros.22820.0270-41371097-0045http://nrs.harvard.edu/urn-3:HUL.InstRepos:41292507BACKGROUND. Inflammation has been hypothesized to play an important etiological role in the initiation or progression of prostate cancer. Circulating levels of the systemic inflammation marker C-reactive protein (CRP) have been associated with increased risk of prostate cancer. We investigated the role of genetic variation in CRP and prostate cancer, under the hypothesis that variants may alter risk of disease.METHODS. We undertook a case-control study nested within the prospective Physicians' Health Study among 1,286 men with incident prostate cancer and 1,264 controls. Four single-nucleotide polymorphisms (SNPs) were selected to capture the common genetic variation across CRP (r(2) > 0.8). We used unconditional logistic regression to assess the association between each SNP and risk of prostate cancer. Linear regression models explored associations between each genotype and plasma CRP levels. RESULTS . None of the CRP SNPs were associated with prostate cancer overall. Individuals with one copy of the minor alleleen-USJournal Article2019-09-0510.1002/pros.22820