Research ExplorerPublicationsGenome-Wide Interaction Analyses between Genetic Variants an...

Genome-Wide Interaction Analyses between Genetic Variants and Alcohol Consumption and Smoking for Risk of Colorectal Cancer

Standard

Genome-Wide Interaction Analyses between Genetic Variants and Alcohol Consumption and Smoking for Risk of Colorectal Cancer. / Gong, Jian; Hutter, Carolyn M; Newcomb, Polly A; Ulrich, Cornelia M; Bien, Stephanie A; Campbell, Peter T; Baron, John A; Berndt, Sonja I; Bezieau, Stephane; Brenner, Hermann; Casey, Graham; Chan, Andrew T; Chang-Claude, Jenny; Du, Mengmeng; Duggan, David; Figueiredo, Jane C; Gallinger, Steven; Giovannucci, Edward L; Haile, Robert W; Harrison, Tabitha A; Hayes, Richard B; Hoffmeister, Michael; Hopper, John L; Hudson, Thomas J; Jeon, Jihyoun; Jenkins, Mark A; Kocarnik, Jonathan; Küry, Sébastien; Le Marchand, Loic; Lin, Yi-Ling; Lindor, Noralane M; Nishihara, Reiko; Ogino, Shuji; Potter, John D; Rudolph, Anja; Schoen, Robert E; Schrotz-King, Petra; Seminara, Daniela; Slattery, Martha L; Thibodeau, Stephen N; Thornquist, Mark; Toth, Reka; Wallace, Robert; White, Emily; Jiao, Shuo; Lemire, Mathieu; Hsu, Li; Peters, Ulrike; GECCO and CCFR.

In: PLOS GENET, Vol. 12, No. 10, 10.2016, p. e1006296.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Gong, J, Hutter, CM, Newcomb, PA, Ulrich, CM, Bien, SA, Campbell, PT, Baron, JA, Berndt, SI, Bezieau, S, Brenner, H, Casey, G, Chan, AT, Chang-Claude, J, Du, M, Duggan, D, Figueiredo, JC, Gallinger, S, Giovannucci, EL, Haile, RW, Harrison, TA, Hayes, RB, Hoffmeister, M, Hopper, JL, Hudson, TJ, Jeon, J, Jenkins, MA, Kocarnik, J, Küry, S, Le Marchand, L, Lin, Y-L, Lindor, NM, Nishihara, R, Ogino, S, Potter, JD, Rudolph, A, Schoen, RE, Schrotz-King, P, Seminara, D, Slattery, ML, Thibodeau, SN, Thornquist, M, Toth, R, Wallace, R, White, E, Jiao, S, Lemire, M, Hsu, L, Peters, U & GECCO and CCFR 2016, 'Genome-Wide Interaction Analyses between Genetic Variants and Alcohol Consumption and Smoking for Risk of Colorectal Cancer', PLOS GENET, vol. 12, no. 10, pp. e1006296. https://doi.org/10.1371/journal.pgen.1006296

APA

Gong, J., Hutter, C. M., Newcomb, P. A., Ulrich, C. M., Bien, S. A., Campbell, P. T., Baron, J. A., Berndt, S. I., Bezieau, S., Brenner, H., Casey, G., Chan, A. T., Chang-Claude, J., Du, M., Duggan, D., Figueiredo, J. C., Gallinger, S., Giovannucci, E. L., Haile, R. W., ... GECCO and CCFR (2016). Genome-Wide Interaction Analyses between Genetic Variants and Alcohol Consumption and Smoking for Risk of Colorectal Cancer. PLOS GENET, 12(10), e1006296. https://doi.org/10.1371/journal.pgen.1006296

Vancouver

Gong J, Hutter CM, Newcomb PA, Ulrich CM, Bien SA, Campbell PT et al. Genome-Wide Interaction Analyses between Genetic Variants and Alcohol Consumption and Smoking for Risk of Colorectal Cancer. PLOS GENET. 2016 Oct;12(10):e1006296. https://doi.org/10.1371/journal.pgen.1006296

Bibtex

@article{7bdad52d1552486f8f5d4818f42f91d0,
title = "Genome-Wide Interaction Analyses between Genetic Variants and Alcohol Consumption and Smoking for Risk of Colorectal Cancer",
abstract = "Genome-wide association studies (GWAS) have identified many genetic susceptibility loci for colorectal cancer (CRC). However, variants in these loci explain only a small proportion of familial aggregation, and there are likely additional variants that are associated with CRC susceptibility. Genome-wide studies of gene-environment interactions may identify variants that are not detected in GWAS of marginal gene effects. To study this, we conducted a genome-wide analysis for interaction between genetic variants and alcohol consumption and cigarette smoking using data from the Colon Cancer Family Registry (CCFR) and the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Interactions were tested using logistic regression. We identified interaction between CRC risk and alcohol consumption and variants in the 9q22.32/HIATL1 (Pinteraction = 1.76×10-8; permuted p-value 3.51x10-8) region. Compared to non-/occasional drinking light to moderate alcohol consumption was associated with a lower risk of colorectal cancer among individuals with rs9409565 CT genotype (OR, 0.82 [95% CI, 0.74-0.91]; P = 2.1×10-4) and TT genotypes (OR,0.62 [95% CI, 0.51-0.75]; P = 1.3×10-6) but not associated among those with the CC genotype (p = 0.059). No genome-wide statistically significant interactions were observed for smoking. If replicated our suggestive finding of a genome-wide significant interaction between genetic variants and alcohol consumption might contribute to understanding colorectal cancer etiology and identifying subpopulations with differential susceptibility to the effect of alcohol on CRC risk.",
keywords = "Aged, Alcohol Drinking, Colorectal Neoplasms, Female, Gene-Environment Interaction, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Male, Membrane Transport Proteins, Middle Aged, Polymorphism, Single Nucleotide, Risk Factors, Smoking, Tumor Suppressor Proteins, Journal Article",
author = "Jian Gong and Hutter, {Carolyn M} and Newcomb, {Polly A} and Ulrich, {Cornelia M} and Bien, {Stephanie A} and Campbell, {Peter T} and Baron, {John A} and Berndt, {Sonja I} and Stephane Bezieau and Hermann Brenner and Graham Casey and Chan, {Andrew T} and Jenny Chang-Claude and Mengmeng Du and David Duggan and Figueiredo, {Jane C} and Steven Gallinger and Giovannucci, {Edward L} and Haile, {Robert W} and Harrison, {Tabitha A} and Hayes, {Richard B} and Michael Hoffmeister and Hopper, {John L} and Hudson, {Thomas J} and Jihyoun Jeon and Jenkins, {Mark A} and Jonathan Kocarnik and S{\'e}bastien K{\"u}ry and {Le Marchand}, Loic and Yi-Ling Lin and Lindor, {Noralane M} and Reiko Nishihara and Shuji Ogino and Potter, {John D} and Anja Rudolph and Schoen, {Robert E} and Petra Schrotz-King and Daniela Seminara and Slattery, {Martha L} and Thibodeau, {Stephen N} and Mark Thornquist and Reka Toth and Robert Wallace and Emily White and Shuo Jiao and Mathieu Lemire and Li Hsu and Ulrike Peters and {GECCO and CCFR}",
year = "2016",
month = oct,
doi = "10.1371/journal.pgen.1006296",
language = "English",
volume = "12",
pages = "e1006296",
journal = "PLOS GENET",
issn = "1553-7404",
publisher = "Public Library of Science",
number = "10",

}

RIS

TY - JOUR

T1 - Genome-Wide Interaction Analyses between Genetic Variants and Alcohol Consumption and Smoking for Risk of Colorectal Cancer

AU - Gong, Jian

AU - Hutter, Carolyn M

AU - Newcomb, Polly A

AU - Ulrich, Cornelia M

AU - Bien, Stephanie A

AU - Campbell, Peter T

AU - Baron, John A

AU - Berndt, Sonja I

AU - Bezieau, Stephane

AU - Brenner, Hermann

AU - Casey, Graham

AU - Chan, Andrew T

AU - Chang-Claude, Jenny

AU - Du, Mengmeng

AU - Duggan, David

AU - Figueiredo, Jane C

AU - Gallinger, Steven

AU - Giovannucci, Edward L

AU - Haile, Robert W

AU - Harrison, Tabitha A

AU - Hayes, Richard B

AU - Hoffmeister, Michael

AU - Hopper, John L

AU - Hudson, Thomas J

AU - Jeon, Jihyoun

AU - Jenkins, Mark A

AU - Kocarnik, Jonathan

AU - Küry, Sébastien

AU - Le Marchand, Loic

AU - Lin, Yi-Ling

AU - Lindor, Noralane M

AU - Nishihara, Reiko

AU - Ogino, Shuji

AU - Potter, John D

AU - Rudolph, Anja

AU - Schoen, Robert E

AU - Schrotz-King, Petra

AU - Seminara, Daniela

AU - Slattery, Martha L

AU - Thibodeau, Stephen N

AU - Thornquist, Mark

AU - Toth, Reka

AU - Wallace, Robert

AU - White, Emily

AU - Jiao, Shuo

AU - Lemire, Mathieu

AU - Hsu, Li

AU - Peters, Ulrike

AU - GECCO and CCFR

PY - 2016/10

Y1 - 2016/10

N2 - Genome-wide association studies (GWAS) have identified many genetic susceptibility loci for colorectal cancer (CRC). However, variants in these loci explain only a small proportion of familial aggregation, and there are likely additional variants that are associated with CRC susceptibility. Genome-wide studies of gene-environment interactions may identify variants that are not detected in GWAS of marginal gene effects. To study this, we conducted a genome-wide analysis for interaction between genetic variants and alcohol consumption and cigarette smoking using data from the Colon Cancer Family Registry (CCFR) and the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Interactions were tested using logistic regression. We identified interaction between CRC risk and alcohol consumption and variants in the 9q22.32/HIATL1 (Pinteraction = 1.76×10-8; permuted p-value 3.51x10-8) region. Compared to non-/occasional drinking light to moderate alcohol consumption was associated with a lower risk of colorectal cancer among individuals with rs9409565 CT genotype (OR, 0.82 [95% CI, 0.74-0.91]; P = 2.1×10-4) and TT genotypes (OR,0.62 [95% CI, 0.51-0.75]; P = 1.3×10-6) but not associated among those with the CC genotype (p = 0.059). No genome-wide statistically significant interactions were observed for smoking. If replicated our suggestive finding of a genome-wide significant interaction between genetic variants and alcohol consumption might contribute to understanding colorectal cancer etiology and identifying subpopulations with differential susceptibility to the effect of alcohol on CRC risk.

AB - Genome-wide association studies (GWAS) have identified many genetic susceptibility loci for colorectal cancer (CRC). However, variants in these loci explain only a small proportion of familial aggregation, and there are likely additional variants that are associated with CRC susceptibility. Genome-wide studies of gene-environment interactions may identify variants that are not detected in GWAS of marginal gene effects. To study this, we conducted a genome-wide analysis for interaction between genetic variants and alcohol consumption and cigarette smoking using data from the Colon Cancer Family Registry (CCFR) and the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Interactions were tested using logistic regression. We identified interaction between CRC risk and alcohol consumption and variants in the 9q22.32/HIATL1 (Pinteraction = 1.76×10-8; permuted p-value 3.51x10-8) region. Compared to non-/occasional drinking light to moderate alcohol consumption was associated with a lower risk of colorectal cancer among individuals with rs9409565 CT genotype (OR, 0.82 [95% CI, 0.74-0.91]; P = 2.1×10-4) and TT genotypes (OR,0.62 [95% CI, 0.51-0.75]; P = 1.3×10-6) but not associated among those with the CC genotype (p = 0.059). No genome-wide statistically significant interactions were observed for smoking. If replicated our suggestive finding of a genome-wide significant interaction between genetic variants and alcohol consumption might contribute to understanding colorectal cancer etiology and identifying subpopulations with differential susceptibility to the effect of alcohol on CRC risk.

KW - Aged

KW - Alcohol Drinking

KW - Colorectal Neoplasms

KW - Female

KW - Gene-Environment Interaction

KW - Genetic Predisposition to Disease

KW - Genome-Wide Association Study

KW - Genotype

KW - Humans

KW - Male

KW - Membrane Transport Proteins

KW - Middle Aged

KW - Polymorphism, Single Nucleotide

KW - Risk Factors

KW - Smoking

KW - Tumor Suppressor Proteins

KW - Journal Article

U2 - 10.1371/journal.pgen.1006296

DO - 10.1371/journal.pgen.1006296

M3 - SCORING: Journal article

C2 - 27723779

VL - 12

SP - e1006296

JO - PLOS GENET

JF - PLOS GENET

SN - 1553-7404

IS - 10

ER -