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Genetic Variation in Base Excision Repair Pathway Genes, Pesticide Exposure, and Prostate Cancer Risk

Background: Previous research indicates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, evidence suggests a role of oxidative DNA damage. Objectives: Because base excision repair (BER) is the predominant pathwa... Full description

Journal Title: Environmental Health Perspectives 2011, Vol.119(12), p.1726-1732
Main Author: Barry, Kathryn Hughes
Other Authors: Koutros, Stella , Berndt, Sonja I , Andreotti, Gabriella , Hoppin, Jane A , Sandler, Dale P , Burdette, Laurie A , Yeager, Meredith , Freeman, Laura E. Beane , Lubin, Jay H , Ma, Xiaomei , Zheng, Tongzhang , Alavanja, Michael C.R
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ID: ISSN: 0091-6765 ; E-ISSN: 1552-9924 ; DOI: 10.1289/ehp.1103454 ; PMCID: 3261977 ; PMID: 21810555
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recordid: pubmed_central3261977
title: Genetic Variation in Base Excision Repair Pathway Genes, Pesticide Exposure, and Prostate Cancer Risk
format: Article
creator:
  • Barry, Kathryn Hughes
  • Koutros, Stella
  • Berndt, Sonja I
  • Andreotti, Gabriella
  • Hoppin, Jane A
  • Sandler, Dale P
  • Burdette, Laurie A
  • Yeager, Meredith
  • Freeman, Laura E. Beane
  • Lubin, Jay H
  • Ma, Xiaomei
  • Zheng, Tongzhang
  • Alavanja, Michael C.R
subjects:
  • Research
  • Dna Repair
  • Gene–Environment Interactions
  • Pesticide
  • Polymorphisms
  • Prostate Cancer
ispartof: Environmental Health Perspectives, 2011, Vol.119(12), p.1726-1732
description: Background: Previous research indicates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, evidence suggests a role of oxidative DNA damage. Objectives: Because base excision repair (BER) is the predominant pathway involved in repairing oxidative damage, we evaluated interactions between 39 pesticides and 394 tag single-nucleotide polymorphisms (SNPs) for 31 BER genes among 776 prostate cancer cases and 1,444 male controls in a nested case–control study of white Agricultural Health Study (AHS) pesticide applicators. Methods: We used likelihood ratio tests from logistic regression models to determine p -values for interactions between three-level pesticide exposure variables (none/low/high) and SNPs (assuming a dominant model), and the false discovery rate (FDR) multiple comparison adjustment approach. Results: The interaction between fonofos and rs1983132 in NEIL3 [nei endonuclease VIII-like 3 ( Escherichia coli )], which encodes a glycosylase that can initiate BER, was the most significant overall [interaction p -value ( p interact ) = 9.3 × 10 –6 ; FDR-adjusted p -value = 0.01]. Fonofos exposure was associated with a monotonic increase in prostate cancer risk among men with CT/TT genotypes for rs1983132 [odds ratios (95% confidence intervals) for low and high use compared with no use were 1.65 (0.91, 3.01) and 3.25 (1.78, 5.92), respectively], whereas fonofos was not associated with prostate cancer risk among men with the CC genotype. Carbofuran and S -ethyl dipropylthiocarbamate (EPTC) interacted similarly with rs1983132; however, these interactions did not meet an FDR < 0.2. Conclusions: Our significant finding regarding fonofos is consistent with previous AHS findings of increased prostate cancer risk with fonofos exposure among those with a family history of prostate cancer. Although requiring replication, our findings suggest a role of BER genetic variation in pesticide-associated prostate cancer risk.
language:
source:
identifier: ISSN: 0091-6765 ; E-ISSN: 1552-9924 ; DOI: 10.1289/ehp.1103454 ; PMCID: 3261977 ; PMID: 21810555
fulltext: fulltext
issn:
  • 0091-6765
  • 00916765
  • 1552-9924
  • 15529924
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titleGenetic Variation in Base Excision Repair Pathway Genes, Pesticide Exposure, and Prostate Cancer Risk
creatorBarry, Kathryn Hughes ; Koutros, Stella ; Berndt, Sonja I ; Andreotti, Gabriella ; Hoppin, Jane A ; Sandler, Dale P ; Burdette, Laurie A ; Yeager, Meredith ; Freeman, Laura E. Beane ; Lubin, Jay H ; Ma, Xiaomei ; Zheng, Tongzhang ; Alavanja, Michael C.R
ispartofEnvironmental Health Perspectives, 2011, Vol.119(12), p.1726-1732
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subjectResearch ; Dna Repair ; Gene–Environment Interactions ; Pesticide ; Polymorphisms ; Prostate Cancer
descriptionBackground: Previous research indicates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, evidence suggests a role of oxidative DNA damage. Objectives: Because base excision repair (BER) is the predominant pathway involved in repairing oxidative damage, we evaluated interactions between 39 pesticides and 394 tag single-nucleotide polymorphisms (SNPs) for 31 BER genes among 776 prostate cancer cases and 1,444 male controls in a nested case–control study of white Agricultural Health Study (AHS) pesticide applicators. Methods: We used likelihood ratio tests from logistic regression models to determine p -values for interactions between three-level pesticide exposure variables (none/low/high) and SNPs (assuming a dominant model), and the false discovery rate (FDR) multiple comparison adjustment approach. Results: The interaction between fonofos and rs1983132 in NEIL3 [nei endonuclease VIII-like 3 ( Escherichia coli )], which encodes a glycosylase that can initiate BER, was the most significant overall [interaction p -value ( p interact ) = 9.3 × 10 –6 ; FDR-adjusted p -value = 0.01]. Fonofos exposure was associated with a monotonic increase in prostate cancer risk among men with CT/TT genotypes for rs1983132 [odds ratios (95% confidence intervals) for low and high use compared with no use were 1.65 (0.91, 3.01) and 3.25 (1.78, 5.92), respectively], whereas fonofos was not associated with prostate cancer risk among men with the CC genotype. Carbofuran and S -ethyl dipropylthiocarbamate (EPTC) interacted similarly with rs1983132; however, these interactions did not meet an FDR < 0.2. Conclusions: Our significant finding regarding fonofos is consistent with previous AHS findings of increased prostate cancer risk with fonofos exposure among those with a family history of prostate cancer. Although requiring replication, our findings suggest a role of BER genetic variation in pesticide-associated prostate cancer risk.
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titleGenetic Variation in Base Excision Repair Pathway Genes, Pesticide Exposure, and Prostate Cancer Risk
descriptionBackground: Previous research indicates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, evidence suggests a role of oxidative DNA damage. Objectives: Because base excision repair (BER) is the predominant pathway involved in repairing oxidative damage, we evaluated interactions between 39 pesticides and 394 tag single-nucleotide polymorphisms (SNPs) for 31 BER genes among 776 prostate cancer cases and 1,444 male controls in a nested case–control study of white Agricultural Health Study (AHS) pesticide applicators. Methods: We used likelihood ratio tests from logistic regression models to determine p -values for interactions between three-level pesticide exposure variables (none/low/high) and SNPs (assuming a dominant model), and the false discovery rate (FDR) multiple comparison adjustment approach. Results: The interaction between fonofos and rs1983132 in NEIL3 [nei endonuclease VIII-like 3 ( Escherichia coli )], which encodes a glycosylase that can initiate BER, was the most significant overall [interaction p -value ( p interact ) = 9.3 × 10 –6 ; FDR-adjusted p -value = 0.01]. Fonofos exposure was associated with a monotonic increase in prostate cancer risk among men with CT/TT genotypes for rs1983132 [odds ratios (95% confidence intervals) for low and high use compared with no use were 1.65 (0.91, 3.01) and 3.25 (1.78, 5.92), respectively], whereas fonofos was not associated with prostate cancer risk among men with the CC genotype. Carbofuran and S -ethyl dipropylthiocarbamate (EPTC) interacted similarly with rs1983132; however, these interactions did not meet an FDR < 0.2. Conclusions: Our significant finding regarding fonofos is consistent with previous AHS findings of increased prostate cancer risk with fonofos exposure among those with a family history of prostate cancer. Although requiring replication, our findings suggest a role of BER genetic variation in pesticide-associated prostate cancer risk.
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abstractBackground: Previous research indicates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, evidence suggests a role of oxidative DNA damage. Objectives: Because base excision repair (BER) is the predominant pathway involved in repairing oxidative damage, we evaluated interactions between 39 pesticides and 394 tag single-nucleotide polymorphisms (SNPs) for 31 BER genes among 776 prostate cancer cases and 1,444 male controls in a nested case–control study of white Agricultural Health Study (AHS) pesticide applicators. Methods: We used likelihood ratio tests from logistic regression models to determine p -values for interactions between three-level pesticide exposure variables (none/low/high) and SNPs (assuming a dominant model), and the false discovery rate (FDR) multiple comparison adjustment approach. Results: The interaction between fonofos and rs1983132 in NEIL3 [nei endonuclease VIII-like 3 ( Escherichia coli )], which encodes a glycosylase that can initiate BER, was the most significant overall [interaction p -value ( p interact ) = 9.3 × 10 –6 ; FDR-adjusted p -value = 0.01]. Fonofos exposure was associated with a monotonic increase in prostate cancer risk among men with CT/TT genotypes for rs1983132 [odds ratios (95% confidence intervals) for low and high use compared with no use were 1.65 (0.91, 3.01) and 3.25 (1.78, 5.92), respectively], whereas fonofos was not associated with prostate cancer risk among men with the CC genotype. Carbofuran and S -ethyl dipropylthiocarbamate (EPTC) interacted similarly with rs1983132; however, these interactions did not meet an FDR < 0.2. Conclusions: Our significant finding regarding fonofos is consistent with previous AHS findings of increased prostate cancer risk with fonofos exposure among those with a family history of prostate cancer. Although requiring replication, our findings suggest a role of BER genetic variation in pesticide-associated prostate cancer risk.
pubNational Institute of Environmental Health Sciences
doi10.1289/ehp.1103454
pmid21810555
pages1726-1732
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date2011-12-00