Search

Your search keyword '"Warnick GS"' showing total 10 results
Start Over Author "Warnick GS"
10 results on '"Warnick GS"'

1. Association of Aspirin and NSAID Use With Risk of Colorectal Cancer According to Genetic Variants

Author

Nan, H, Hutter, CM, Lin, Y, Jacobs, EJ, Ulrich, CM, White, E, Baron, JA, Berndt, SI, Brenner, H, Butterbach, K, Caan, BJ, Campbell, PT, Carlson, CS, Casey, G, Chang-Claude, J, Chanock, SJ, Cotterchio, M, Duggan, D, Figueiredo, JC, Fuchs, CS, Giovannucci, EL, Gong, J, Haile, RW, Harrison, TA, Hayes, RB, Hoffmeister, M, Hopper, JL, Hudson, TJ, Jenkins, MA, Jiao, S, Lindor, NM, Lemire, M, Le Marchand, L, Newcomb, PA, Ogino, S, Pflugeisen, BM, Potter, JD, Qu, C, Rosse, SA, Rudolph, A, Schoen, RE, Schumacher, FR, Seminara, D, Slattery, ML, Thibodeau, SN, Thomas, F, Thornquist, M, Warnick, GS, Zanke, BW, Gauderman, WJ, Peters, U, Hsu, L, Chan, AT, Nan, H, Hutter, CM, Lin, Y, Jacobs, EJ, Ulrich, CM, White, E, Baron, JA, Berndt, SI, Brenner, H, Butterbach, K, Caan, BJ, Campbell, PT, Carlson, CS, Casey, G, Chang-Claude, J, Chanock, SJ, Cotterchio, M, Duggan, D, Figueiredo, JC, Fuchs, CS, Giovannucci, EL, Gong, J, Haile, RW, Harrison, TA, Hayes, RB, Hoffmeister, M, Hopper, JL, Hudson, TJ, Jenkins, MA, Jiao, S, Lindor, NM, Lemire, M, Le Marchand, L, Newcomb, PA, Ogino, S, Pflugeisen, BM, Potter, JD, Qu, C, Rosse, SA, Rudolph, A, Schoen, RE, Schumacher, FR, Seminara, D, Slattery, ML, Thibodeau, SN, Thomas, F, Thornquist, M, Warnick, GS, Zanke, BW, Gauderman, WJ, Peters, U, Hsu, L, and Chan, AT

Abstract

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

Published
2015

2. Gene-Environment Interaction Involving Recently Identified Colorectal Cancer Susceptibility Loci

Author

Kantor, ED, Hutter, CM, Minnier, J, Berndt, SI, Brenner, H, Caan, BJ, Campbell, PT, Carlson, CS, Casey, G, Chan, AT, Chang-Claude, J, Chanock, SJ, Cotterchio, M, Du, M, Duggan, D, Fuchs, CS, Giovannucci, EL, Gong, J, Harrison, TA, Hayes, RB, Henderson, BE, Hoffmeister, M, Hopper, JL, Jenkins, MA, Jiao, S, Kolonel, LN, Le Marchand, L, Lemire, M, Ma, J, Newcomb, PA, Ochs-Balcom, HM, Pflugeisen, BM, Potter, JD, Rudolph, A, Schoen, RE, Seminara, D, Slattery, ML, Stelling, DL, Thomas, F, Thornquist, M, Ulrich, CM, Warnick, GS, Zanke, BW, Peters, U, Hsu, L, White, E, Kantor, ED, Hutter, CM, Minnier, J, Berndt, SI, Brenner, H, Caan, BJ, Campbell, PT, Carlson, CS, Casey, G, Chan, AT, Chang-Claude, J, Chanock, SJ, Cotterchio, M, Du, M, Duggan, D, Fuchs, CS, Giovannucci, EL, Gong, J, Harrison, TA, Hayes, RB, Henderson, BE, Hoffmeister, M, Hopper, JL, Jenkins, MA, Jiao, S, Kolonel, LN, Le Marchand, L, Lemire, M, Ma, J, Newcomb, PA, Ochs-Balcom, HM, Pflugeisen, BM, Potter, JD, Rudolph, A, Schoen, RE, Seminara, D, Slattery, ML, Stelling, DL, Thomas, F, Thornquist, M, Ulrich, CM, Warnick, GS, Zanke, BW, Peters, U, Hsu, L, and White, E

Abstract

BACKGROUND: Genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) that are associated with risk of colorectal cancer. Prior research has evaluated the presence of gene-environment interaction involving the first 10 identified susceptibility loci, but little work has been conducted on interaction involving SNPs at recently identified susceptibility loci, including: rs10911251, rs6691170, rs6687758, rs11903757, rs10936599, rs647161, rs1321311, rs719725, rs1665650, rs3824999, rs7136702, rs11169552, rs59336, rs3217810, rs4925386, and rs2423279. METHODS: Data on 9,160 cases and 9,280 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) and Colon Cancer Family Registry (CCFR) were used to evaluate the presence of interaction involving the above-listed SNPs and sex, body mass index (BMI), alcohol consumption, smoking, aspirin use, postmenopausal hormone (PMH) use, as well as intake of dietary calcium, dietary fiber, dietary folate, red meat, processed meat, fruit, and vegetables. Interaction was evaluated using a fixed effects meta-analysis of an efficient Empirical Bayes estimator, and permutation was used to account for multiple comparisons. RESULTS: None of the permutation-adjusted P values reached statistical significance. CONCLUSIONS: The associations between recently identified genetic susceptibility loci and colorectal cancer are not strongly modified by sex, BMI, alcohol, smoking, aspirin, PMH use, and various dietary factors. IMPACT: Results suggest no evidence of strong gene-environment interactions involving the recently identified 16 susceptibility loci for colorectal cancer taken one at a time.

Published
2014

3. Genome-Wide Diet-Gene Interaction Analyses for Risk of Colorectal Cancer

Author

Amos, CI, Figueiredo, JC, Hsu, L, Hutter, CM, Lin, Y, Campbell, PT, Baron, JA, Berndt, SI, Jiao, S, Casey, G, Fortini, B, Chan, AT, Cotterchio, M, Lemire, M, Gallinger, S, Harrison, TA, Le Marchand, L, Newcomb, PA, Slattery, ML, Caan, BJ, Carlson, CS, Zanke, BW, Rosse, SA, Brenner, H, Giovannucci, EL, Wu, K, Chang-Claude, J, Chanock, SJ, Curtis, KR, Duggan, D, Gong, J, Haile, RW, Hayes, RB, Hoffmeister, M, Hopper, JL, Jenkins, MA, Kolonel, LN, Qu, C, Rudolph, A, Schoen, RE, Schumacher, FR, Seminara, D, Stelling, DL, Thibodeau, SN, Thornquist, M, Warnick, GS, Henderson, BE, Ulrich, C, Gauderman, WJ, Potter, JD, White, E, Peters, U, Amos, CI, Figueiredo, JC, Hsu, L, Hutter, CM, Lin, Y, Campbell, PT, Baron, JA, Berndt, SI, Jiao, S, Casey, G, Fortini, B, Chan, AT, Cotterchio, M, Lemire, M, Gallinger, S, Harrison, TA, Le Marchand, L, Newcomb, PA, Slattery, ML, Caan, BJ, Carlson, CS, Zanke, BW, Rosse, SA, Brenner, H, Giovannucci, EL, Wu, K, Chang-Claude, J, Chanock, SJ, Curtis, KR, Duggan, D, Gong, J, Haile, RW, Hayes, RB, Hoffmeister, M, Hopper, JL, Jenkins, MA, Kolonel, LN, Qu, C, Rudolph, A, Schoen, RE, Schumacher, FR, Seminara, D, Stelling, DL, Thibodeau, SN, Thornquist, M, Warnick, GS, Henderson, BE, Ulrich, C, Gauderman, WJ, Potter, JD, White, E, and Peters, U

Abstract

Dietary factors, including meat, fruits, vegetables and fiber, are associated with colorectal cancer; however, there is limited information as to whether these dietary factors interact with genetic variants to modify risk of colorectal cancer. We tested interactions between these dietary factors and approximately 2.7 million genetic variants for colorectal cancer risk among 9,287 cases and 9,117 controls from ten studies. We used logistic regression to investigate multiplicative gene-diet interactions, as well as our recently developed Cocktail method that involves a screening step based on marginal associations and gene-diet correlations and a testing step for multiplicative interactions, while correcting for multiple testing using weighted hypothesis testing. Per quartile increment in the intake of red and processed meat were associated with statistically significant increased risks of colorectal cancer and vegetable, fruit and fiber intake with lower risks. From the case-control analysis, we detected a significant interaction between rs4143094 (10p14/near GATA3) and processed meat consumption (OR = 1.17; p = 8.7E-09), which was consistently observed across studies (p heterogeneity = 0.78). The risk of colorectal cancer associated with processed meat was increased among individuals with the rs4143094-TG and -TT genotypes (OR = 1.20 and OR = 1.39, respectively) and null among those with the GG genotype (OR = 1.03). Our results identify a novel gene-diet interaction with processed meat for colorectal cancer, highlighting that diet may modify the effect of genetic variants on disease risk, which may have important implications for prevention.

Published
2014

4. Genome-Wide Diet-Gene Interaction Analyses for Risk of Colorectal Cancer

Author

Figueiredo, JC, Hsu, L, Hutter, CM, Lin, Y, Campbell, PT, Baron, JA, Berndt, SI, Jiao, S, Casey, G, Fortini, B, Chan, AT, Cotterchio, M, Lemire, M, Gallinger, S, Harrison, TA, Le Marchand, L, Newcomb, PA, Slattery, ML, Caan, BJ, Carlson, CS, Zanke, BW, Rosse, SA, Brenner, H, Giovannucci, EL, Wu, K, Chang-Claude, J, Chanock, SJ, Curtis, KR, Duggan, D, Gong, J, Haile, RW, Hayes, RB, Hoffmeister, M, Hopper, JL, Jenkins, MA, Kolonel, LN, Qu, C, Rudolph, A, Schoen, RE, Schumacher, FR, Seminara, D, Stelling, DL, Thibodeau, SN, Thornquist, M, Warnick, GS, Henderson, BE, Ulrich, CM, Gauderman, WJ, Potter, JD, White, E, Peters, U, Figueiredo, JC, Hsu, L, Hutter, CM, Lin, Y, Campbell, PT, Baron, JA, Berndt, SI, Jiao, S, Casey, G, Fortini, B, Chan, AT, Cotterchio, M, Lemire, M, Gallinger, S, Harrison, TA, Le Marchand, L, Newcomb, PA, Slattery, ML, Caan, BJ, Carlson, CS, Zanke, BW, Rosse, SA, Brenner, H, Giovannucci, EL, Wu, K, Chang-Claude, J, Chanock, SJ, Curtis, KR, Duggan, D, Gong, J, Haile, RW, Hayes, RB, Hoffmeister, M, Hopper, JL, Jenkins, MA, Kolonel, LN, Qu, C, Rudolph, A, Schoen, RE, Schumacher, FR, Seminara, D, Stelling, DL, Thibodeau, SN, Thornquist, M, Warnick, GS, Henderson, BE, Ulrich, CM, Gauderman, WJ, Potter, JD, White, E, and Peters, U

Abstract

Dietary factors, including meat, fruits, vegetables and fiber, are associated with colorectal cancer; however, there is limited information as to whether these dietary factors interact with genetic variants to modify risk of colorectal cancer. We tested interactions between these dietary factors and approximately 2.7 million genetic variants for colorectal cancer risk among 9,287 cases and 9,117 controls from ten studies. We used logistic regression to investigate multiplicative gene-diet interactions, as well as our recently developed Cocktail method that involves a screening step based on marginal associations and gene-diet correlations and a testing step for multiplicative interactions, while correcting for multiple testing using weighted hypothesis testing. Per quartile increment in the intake of red and processed meat were associated with statistically significant increased risks of colorectal cancer and vegetable, fruit and fiber intake with lower risks. From the case-control analysis, we detected a significant interaction between rs4143094 (10p14/near GATA3) and processed meat consumption (OR = 1.17; p = 8.7E-09), which was consistently observed across studies (p heterogeneity = 0.78). The risk of colorectal cancer associated with processed meat was increased among individuals with the rs4143094-TG and -TT genotypes (OR = 1.20 and OR = 1.39, respectively) and null among those with the GG genotype (OR = 1.03). Our results identify a novel gene-diet interaction with processed meat for colorectal cancer, highlighting that diet may modify the effect of genetic variants on disease risk, which may have important implications for prevention. © 2014.

Published
2014

5. Derivation and Validation of a Risk Assessment Model for Immunomodulatory Drug-Associated Thrombosis Among Patients With Multiple Myeloma.

Author

Li A, Wu Q, Luo S, Warnick GS, Zakai NA, Libby EN, Gage BF, Garcia DA, Lyman GH, and Sanfilippo KM

Subjects
Aged, Aged, 80 and over, Databases, Factual, Female, Humans, Immunologic Factors adverse effects, Immunologic Factors therapeutic use, Male, Medicare, Middle Aged, Multiple Myeloma complications, Multiple Myeloma epidemiology, Multiple Myeloma pathology, Proportional Hazards Models, Risk Assessment, Risk Factors, United States epidemiology, Venous Thromboembolism chemically induced, Venous Thromboembolism epidemiology, Venous Thromboembolism pathology, Venous Thrombosis chemically induced, Venous Thrombosis epidemiology, Venous Thrombosis pathology, Anticoagulants therapeutic use, Multiple Myeloma drug therapy, Venous Thromboembolism drug therapy, Venous Thrombosis drug therapy
Abstract

Background: Although venous thromboembolism (VTE) is a significant complication for patients with multiple myeloma (MM) receiving immunomodulatory drugs (IMiDs), no validated clinical model predicts VTE in this population. This study aimed to derive and validate a new risk assessment model (RAM) for IMiD-associated VTE., Methods: Patients with newly diagnosed MM receiving IMiDs were selected from the SEER-Medicare database (n=2,397) to derive a RAM and then data from the Veterans Health Administration database (n=1,251) were used to externally validate the model. A multivariable cause-specific Cox regression model was used for model development., Results: The final RAM, named the "SAVED" score, included 5 clinical variables: prior surgery, Asian race, VTE history, age ≥80 years, and dexamethasone dose. The model stratified approximately 30% of patients in both the derivation and the validation cohorts as high-risk. Hazard ratios (HRs) were 1.85 (P<.01) and 1.98 (P<.01) for high- versus low-risk groups in the derivation and validation cohorts, respectively. In contrast, the method of stratification recommended in the current NCCN Guidelines for Cancer-Associated Venous Thromboembolic Disease had HRs of 1.21 (P=.17) and 1.41 (P=.07) for the corresponding risk groups in the 2 datasets., Conclusions: The SAVED score outperformed the current NCCN Guidelines in risk-stratification of patients with MM receiving IMiD therapy. This clinical model can help inform providers and patients of VTE risk before IMiD initiation and provides a simplified clinical backbone for further prognostic biomarker development in this population.

Published
2019
Full Text
View/download PDF

6. CYP24A1 variant modifies the association between use of oestrogen plus progestogen therapy and colorectal cancer risk.

Author

Garcia-Albeniz X, Rudolph A, Hutter C, White E, Lin Y, Rosse SA, Figueiredo JC, Harrison TA, Jiao S, Brenner H, Casey G, Hudson TJ, Thornquist M, Le Marchand L, Potter J, Slattery ML, Zanke B, Baron JA, Caan BJ, Chanock SJ, Berndt SI, Stelling D, Fuchs CS, Hoffmeister M, Butterbach K, Du M, James Gauderman W, Gunter MJ, Lemire M, Ogino S, Lin J, Hayes RB, Haile RW, Schoen RE, Warnick GS, Jenkins MA, Thibodeau SN, Schumacher FR, Lindor NM, Kolonel LN, Hopper JL, Gong J, Seminara D, Pflugeisen BM, Ulrich CM, Qu C, Duggan D, Cotterchio M, Campbell PT, Carlson CS, Newcomb PA, Giovannucci E, Hsu L, Chan AT, Peters U, and Chang-Claude J

Subjects
Adenocarcinoma epidemiology, Aged, Bayes Theorem, Case-Control Studies, Colorectal Neoplasms epidemiology, Drug Therapy, Combination, Female, Gene-Environment Interaction, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Logistic Models, Middle Aged, Polymorphism, Single Nucleotide, Risk Factors, Adenocarcinoma genetics, Colorectal Neoplasms genetics, Estrogen Replacement Therapy methods, Estrogens therapeutic use, Progestins therapeutic use, Vitamin D3 24-Hydroxylase genetics
Abstract

Background: Menopausal hormone therapy (MHT) use has been consistently associated with a decreased risk of colorectal cancer (CRC) in women. Our aim was to use a genome-wide gene-environment interaction analysis to identify genetic modifiers of CRC risk associated with use of MHT., Methods: We included 10 835 postmenopausal women (5419 cases and 5416 controls) from 10 studies. We evaluated use of any MHT, oestrogen-only (E-only) and combined oestrogen-progestogen (E+P) hormone preparations. To test for multiplicative interactions, we applied the empirical Bayes (EB) test as well as the Wald test in conventional case-control logistic regression as primary tests. The Cocktail test was used as secondary test., Results: The EB test identified a significant interaction between rs964293 at 20q13.2/CYP24A1 and E+P (interaction OR (95% CIs)=0.61 (0.52-0.72), P=4.8 × 10(-9)). The secondary analysis also identified this interaction (Cocktail test OR=0.64 (0.52-0.78), P=1.2 × 10(-5) (alpha threshold=3.1 × 10(-4)). The ORs for association between E+P and CRC risk by rs964293 genotype were as follows: C/C, 0.96 (0.61-1.50); A/C, 0.61 (0.39-0.95) and A/A, 0.40 (0.22-0.73), respectively., Conclusions: Our results indicate that rs964293 modifies the association between E+P and CRC risk. The variant is located near CYP24A1, which encodes an enzyme involved in vitamin D metabolism. This novel finding offers additional insight into downstream pathways of CRC etiopathogenesis.

Published
2016
Full Text
View/download PDF

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

Author

Nan H, Hutter CM, Lin Y, Jacobs EJ, Ulrich CM, White E, Baron JA, Berndt SI, Brenner H, Butterbach K, Caan BJ, Campbell PT, Carlson CS, Casey G, Chang-Claude J, Chanock SJ, Cotterchio M, Duggan D, Figueiredo JC, Fuchs CS, Giovannucci EL, Gong J, Haile RW, Harrison TA, Hayes RB, Hoffmeister M, Hopper JL, Hudson TJ, Jenkins MA, Jiao S, Lindor NM, Lemire M, Le Marchand L, Newcomb PA, Ogino S, Pflugeisen BM, Potter JD, Qu C, Rosse SA, Rudolph A, Schoen RE, Schumacher FR, Seminara D, Slattery ML, Thibodeau SN, Thomas F, Thornquist M, Warnick GS, Zanke BW, Gauderman WJ, Peters U, Hsu L, and Chan AT

Subjects
Case-Control Studies, Chromosomes, Human, Pair 12, Chromosomes, Human, Pair 15, Colorectal Neoplasms genetics, Female, Genetic Markers, Genotype, Humans, Male, Risk Factors, Anti-Inflammatory Agents, Non-Steroidal therapeutic use, Aspirin therapeutic use, Colorectal Neoplasms prevention & control, Gene-Environment Interaction, Polymorphism, Single Nucleotide
Abstract

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.

Published
2015
Full Text
View/download PDF

8. Gene-environment interaction involving recently identified colorectal cancer susceptibility Loci.

Author

Kantor ED, Hutter CM, Minnier J, Berndt SI, Brenner H, Caan BJ, Campbell PT, Carlson CS, Casey G, Chan AT, Chang-Claude J, Chanock SJ, Cotterchio M, Du M, Duggan D, Fuchs CS, Giovannucci EL, Gong J, Harrison TA, Hayes RB, Henderson BE, Hoffmeister M, Hopper JL, Jenkins MA, Jiao S, Kolonel LN, Le Marchand L, Lemire M, Ma J, Newcomb PA, Ochs-Balcom HM, Pflugeisen BM, Potter JD, Rudolph A, Schoen RE, Seminara D, Slattery ML, Stelling DL, Thomas F, Thornquist M, Ulrich CM, Warnick GS, Zanke BW, Peters U, Hsu L, and White E

Subjects
Adult, Aged, Aged, 80 and over, Case-Control Studies, Diet statistics & numerical data, Female, Genetic Predisposition to Disease, Genotype, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Risk Factors, Young Adult, Colorectal Neoplasms epidemiology, Colorectal Neoplasms genetics, Gene-Environment Interaction, Genome-Wide Association Study methods
Abstract

Background: Genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) that are associated with risk of colorectal cancer. Prior research has evaluated the presence of gene-environment interaction involving the first 10 identified susceptibility loci, but little work has been conducted on interaction involving SNPs at recently identified susceptibility loci, including: rs10911251, rs6691170, rs6687758, rs11903757, rs10936599, rs647161, rs1321311, rs719725, rs1665650, rs3824999, rs7136702, rs11169552, rs59336, rs3217810, rs4925386, and rs2423279., Methods: Data on 9,160 cases and 9,280 controls from the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) and Colon Cancer Family Registry (CCFR) were used to evaluate the presence of interaction involving the above-listed SNPs and sex, body mass index (BMI), alcohol consumption, smoking, aspirin use, postmenopausal hormone (PMH) use, as well as intake of dietary calcium, dietary fiber, dietary folate, red meat, processed meat, fruit, and vegetables. Interaction was evaluated using a fixed effects meta-analysis of an efficient Empirical Bayes estimator, and permutation was used to account for multiple comparisons., Results: None of the permutation-adjusted P values reached statistical significance., Conclusions: The associations between recently identified genetic susceptibility loci and colorectal cancer are not strongly modified by sex, BMI, alcohol, smoking, aspirin, PMH use, and various dietary factors., Impact: Results suggest no evidence of strong gene-environment interactions involving the recently identified 16 susceptibility loci for colorectal cancer taken one at a time., (©2014 American Association for Cancer Research.)

Published
2014
Full Text
View/download PDF

9. Genome-wide diet-gene interaction analyses for risk of colorectal cancer.

Author

Figueiredo JC, Hsu L, Hutter CM, Lin Y, Campbell PT, Baron JA, Berndt SI, Jiao S, Casey G, Fortini B, Chan AT, Cotterchio M, Lemire M, Gallinger S, Harrison TA, Le Marchand L, Newcomb PA, Slattery ML, Caan BJ, Carlson CS, Zanke BW, Rosse SA, Brenner H, Giovannucci EL, Wu K, Chang-Claude J, Chanock SJ, Curtis KR, Duggan D, Gong J, Haile RW, Hayes RB, Hoffmeister M, Hopper JL, Jenkins MA, Kolonel LN, Qu C, Rudolph A, Schoen RE, Schumacher FR, Seminara D, Stelling DL, Thibodeau SN, Thornquist M, Warnick GS, Henderson BE, Ulrich CM, Gauderman WJ, Potter JD, White E, and Peters U

Subjects
Adult, Aged, Case-Control Studies, Dietary Fiber administration & dosage, Female, Fruit, Genome-Wide Association Study methods, Genotype, Humans, Male, Meat adverse effects, Middle Aged, Polymorphism, Single Nucleotide genetics, Risk, Risk Factors, Vegetables, Young Adult, Colorectal Neoplasms etiology, Colorectal Neoplasms genetics, Diet adverse effects
Abstract

Dietary factors, including meat, fruits, vegetables and fiber, are associated with colorectal cancer; however, there is limited information as to whether these dietary factors interact with genetic variants to modify risk of colorectal cancer. We tested interactions between these dietary factors and approximately 2.7 million genetic variants for colorectal cancer risk among 9,287 cases and 9,117 controls from ten studies. We used logistic regression to investigate multiplicative gene-diet interactions, as well as our recently developed Cocktail method that involves a screening step based on marginal associations and gene-diet correlations and a testing step for multiplicative interactions, while correcting for multiple testing using weighted hypothesis testing. Per quartile increment in the intake of red and processed meat were associated with statistically significant increased risks of colorectal cancer and vegetable, fruit and fiber intake with lower risks. From the case-control analysis, we detected a significant interaction between rs4143094 (10p14/near GATA3) and processed meat consumption (OR = 1.17; p = 8.7E-09), which was consistently observed across studies (p heterogeneity = 0.78). The risk of colorectal cancer associated with processed meat was increased among individuals with the rs4143094-TG and -TT genotypes (OR = 1.20 and OR = 1.39, respectively) and null among those with the GG genotype (OR = 1.03). Our results identify a novel gene-diet interaction with processed meat for colorectal cancer, highlighting that diet may modify the effect of genetic variants on disease risk, which may have important implications for prevention.

Published
2014
Full Text
View/download PDF

10. Characterization of gene-environment interactions for colorectal cancer susceptibility loci.

Author

Hutter CM, Chang-Claude J, Slattery ML, Pflugeisen BM, Lin Y, Duggan D, Nan H, Lemire M, Rangrej J, Figueiredo JC, Jiao S, Harrison TA, Liu Y, Chen LS, Stelling DL, Warnick GS, Hoffmeister M, Küry S, Fuchs CS, Giovannucci E, Hazra A, Kraft P, Hunter DJ, Gallinger S, Zanke BW, Brenner H, Frank B, Ma J, Ulrich CM, White E, Newcomb PA, Kooperberg C, LaCroix AZ, Prentice RL, Jackson RD, Schoen RE, Chanock SJ, Berndt SI, Hayes RB, Caan BJ, Potter JD, Hsu L, Bézieau S, Chan AT, Hudson TJ, and Peters U

Subjects
Diet, Genotype, Humans, Polymorphism, Single Nucleotide, Colorectal Neoplasms genetics, Gene-Environment Interaction, Genetic Predisposition to Disease genetics
Abstract

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 at 8q23.3 (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 × 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.

Published
2012
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results