Association of aspirin and NSAID use with risk of colorectal cancer according to genetic variants.

Autor:	Nan H; Department of Epidemiology, Richard M. Fairbanks School of Public Health, Indiana University, Indianapolis2Indiana University Melvin and Bren Simon Cancer Center, Indianapolis., Hutter CM; National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland., Lin Y; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Jacobs EJ; Epidemiology Research Program, American Cancer Society, Atlanta, Georgia., Ulrich CM; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington6Huntsman Cancer Institute, University of Utah, Salt Lake City., White E; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington7Department of Epidemiology, University of Washington School of Public Health, Seattle., Baron JA; Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill., Berndt SI; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland., Brenner H; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany11German Cancer Consortium (DKTK), Heidelberg, Germany., Butterbach K; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany., Caan BJ; Division of Research, Kaiser Permanente Medical Care Program of Northern California, Oakland., Campbell PT; Epidemiology Research Program, American Cancer Society, Atlanta, Georgia., Carlson CS; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Casey G; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles., Chang-Claude J; Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany., Chanock SJ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland., Cotterchio M; Prevention and Cancer Control, Cancer Care Ontario, Toronto, Ontario, Canada., Duggan D; Genetic Basis of Human Disease Division, Translational Genomics Research Institute (TGen), Phoenix, Arizona., Figueiredo JC; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles., Fuchs CS; Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts., Giovannucci EL; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massacusetts., Gong J; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Haile RW; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles., Harrison TA; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Hayes RB; Division of Epidemiology, Department of Population Health, New York University School of Medicine, New York, New York., Hoffmeister M; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany., Hopper JL; Melbourne School of Population Health, University of Melbourne, Victoria, Australia., Hudson TJ; Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada22Ontario Institute for Cancer Research, Toronto, Ontario, Canada., Jenkins MA; Melbourne School of Population Health, University of Melbourne, Victoria, Australia., Jiao S; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Lindor NM; Department of Health Sciences Research, Mayo Clinic, Scottsdale, Arizona., Lemire M; Ontario Institute for Cancer Research, Toronto, Ontario, Canada., Le Marchand L; Epidemiology Program, University of Hawaii Cancer Center, Honolulu., Newcomb PA; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Ogino S; Department of Medical Oncology, Dana Farber Cancer Institute, Boston, Massachusetts25Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts26Department of Epidemiology, Harvard School of Public Health, Boston, Masschusetts., Pflugeisen BM; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Potter JD; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington27Centre for Public Health Research, Massey University, Wellington, New Zealand., Qu C; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Rosse SA; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Rudolph A; Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany., Schoen RE; Department of Medicine and Epidemiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania., Schumacher FR; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles., Seminara D; National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland., Slattery ML; Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City., Thibodeau SN; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota31Department of Medical Genetics, Mayo Clinic, Rochester, Minnesota., Thomas F; Division of Biostatistics and Epidemiology, Department of Preventive Medicine, University of Tennessee Healthy Science Center, Memphis., Thornquist M; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Warnick GS; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington., Zanke BW; Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada., Gauderman WJ; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles., Peters U; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington7Department of Epidemiology, University of Washington School of Public Health, Seattle., Hsu L; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington34Department of Biostatistics, University of Washington, Seattle., Chan AT; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massacusetts35Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Jazyk:	angličtina
Zdroj:	JAMA [JAMA] 2015 Mar 17; Vol. 313 (11), pp. 1133-42.
DOI:	10.1001/jama.2015.1815
Abstrakt:	Importance: Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer. Objective: To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene × environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer. Design, Setting, and Participants: Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011. Participants were all of European descent. Exposures: Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors. Main Outcomes and Measures: Colorectal cancer. Results: Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% CI, 0.64-0.74]; P = 6.2 × 10(-28)) compared with nonregular use. In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 × 10(-9) for interaction). Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P = 7.7 × 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% CI, 1.27-2.81]; P = .002). In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 × 10(-9) for interaction). Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 × 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% CI, 0.78-1.20]; P = .76). Conclusions and Relevance: In this genome-wide investigation of gene × environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15. Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies.
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu