Characterization of Gene-Environment Interactions for Colorectal Cancer Susceptibility Loci

被引：147

作者：

Hutter, Carolyn M. ^{[1
,2
]}

Chang-Claude, Jenny ^{[4
]}

Slattery, Martha L. ^{[7
]}

Pflugeisen, Bethann M. ^{[1
]}

Lin, Yi ^{[1
]}

Duggan, David ^{[8
]}

Nan, Hongmei ^{[9
,10
,11
]}

Lemire, Mathieu ^{[15
]}

Rangrej, Jagadish ^{[15
]}

Figueiredo, Jane C. ^{[19
]}

Jiao, Shuo ^{[1
]}

Harrison, Tabitha A. ^{[1
]}

Liu, Yan ^{[20
]}

Chen, Lin S. ^{[21
]}

Stelling, Deanna L. ^{[1
]}

Warnick, Greg S. ^{[1
]}

Hoffmeister, Michael ^{[5
]}

Kuery, Sebastien ^{[22
]}

Fuchs, Charles S. ^{[9
,10
,13
]}

Giovannucci, Edward ^{[9
,10
,12
]}

Hazra, Aditi ^{[9
,10
,11
]}

Kraft, Peter ^{[11
]}

Hunter, David J. ^{[11
]}

Gallinger, Steven ^{[16
]}

Zanke, Brent W. ^{[23
]}

Brenner, Hermann ^{[5
]}

Frank, Bernd ^{[5
]}

Ma, Jing ^{[9
,10
]}

Ulrich, Cornelia M. ^{[1
,2
,6
]}

White, Emily ^{[1
,2
]}

Newcomb, Polly A. ^{[1
,2
]}

Kooperberg, Charles ^{[1
,3
]}

LaCroix, Andrea Z. ^{[1
]}

Prentice, Ross L. ^{[1
]}

Jackson, Rebecca D. ^{[24
]}

Schoen, Robert E. ^{[25
]}

Chanock, Stephen J. ^{[26
]}

Berndt, Sonja I. ^{[26
]}

Hayes, Richard B. ^{[27
]}

Caan, Bette J. ^{[28
]}

Potter, John D. ^{[1
,2
,29
]}

Hsu, Li ^{[1
,3
]}

Bezieau, Stephane ^{[22
]}

Chan, Andrew T. ^{[9
,10
,14
]}

Hudson, Thomas J. ^{[15
,17
,18
]}

Peters, Ulrike ^{[1
,2
]}

机构：

[1] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA

[2] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA

[3] Univ Washington, Dept Biostat, Seattle, WA 98195 USA

[4] German Canc Res Ctr, Div Canc Epidemiol, D-6900 Heidelberg, Germany

[5] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-6900 Heidelberg, Germany

[6] German Canc Res Ctr, Div Prevent Oncol, D-6900 Heidelberg, Germany

[7] Univ Utah, Dept Internal Med, Hlth Sci Ctr, Salt Lake City, UT 84112 USA

[8] Translat Genom Res Inst, Phoenix, AZ USA

[9] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA

[10] Harvard Univ, Sch Med, Boston, MA USA

[11] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02115 USA

[12] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA

[13] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA

[14] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA

[15] Ontario Inst Canc Res, Toronto, ON, Canada

[16] Toronto Gen Hosp, Univ Hlth Network, Dept Surg, Toronto, ON, Canada

[17] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada

[18] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada

[19] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA

[20] Stephens & Associates, Carrollton, TX USA

[21] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA

[22] CHU Nantes, Serv Genet Med, F-44035 Nantes 01, France

[23] Ottawa Hosp Res Inst, Clin Epidemiol Program, Ottawa, ON, Canada

[24] Ohio State Univ, Div Endocrinol Diabet & Metab, Columbus, OH 43210 USA

[25] Univ Pittsburgh, Dept Epidemiol, Med Ctr, Pittsburgh, PA 15261 USA

[26] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA

[27] NYU, Sch Med, Dept Environm Med, Div Epidemiol, New York, NY USA

[28] Kaiser Permanente Med Care Program, Div Res, Oakland, CA 94611 USA

[29] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand

来源：

CANCER RESEARCH | 2012年 / 72卷 / 08期

基金：

加拿大健康研究院; 美国国家卫生研究院;

关键词：

GENOME-WIDE ASSOCIATION; COLON-CANCER; LIFE-STYLE; RISK; METAANALYSIS; VARIANTS; HEALTH; FRUIT; SCAN; 8Q24;

D O I：

10.1158/0008-5472.CAN-11-4067

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Genome-wide association studies (GWAS) have identified more than a dozen loci associated with colorectal cancer (CRC) risk. Here, we examined potential effect-modification between single-nucleotide polymorphisms (SNP) at 10 of these loci and probable or established environmental risk factors for CRC in 7,016 CRC cases and 9,723 controls from nine cohort and case-control studies. We used meta-analysis of an efficient empirical-Bayes estimator to detect potential multiplicative interactions between each of the SNPs [rs16892766 at8q23.3 (EIF3H/UTP23), rs6983267 at 8q24 (MYC), rs10795668 at 10p14 (FLJ3802842), rs3802842 at 11q23 (LOC120376), rs4444235 at 14q22.2 (BMP4), rs4779584 at 15q13 (GREM1), rs9929218 at 16q22.1 (CDH1), rs4939827 at 18q21 (SMAD7), rs10411210 at 19q13.1 (RHPN2), and rs961253 at 20p12.3 (BMP2)] and select major CRC risk factors (sex, body mass index, height, smoking status, aspirin/nonsteroidal anti-inflammatory drug use, alcohol use, and dietary intake of calcium, folate, red meat, processed meat, vegetables, fruit, and fiber). The strongest statistical evidence for a gene-environment interaction across studies was for vegetable consumption and rs16892766, located on chromosome 8q23.3, near the EIF3H and UTP23 genes (nominal P-interaction = 1.3 x 10(-4); adjusted P = 0.02). The magnitude of the main effect of the SNP increased with increasing levels of vegetable consumption. No other interactions were statistically significant after adjusting for multiple comparisons. Overall, the association of most CRC susceptibility loci identified in initial GWAS seems to be invariant to the other risk factors considered; however, our results suggest potential modification of the rs16892766 effect by vegetable consumption. Cancer Res; 72(8); 2036-44. (C) 2012 AACR.

引用

页码：2036 / 2044

页数：9

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