Polymorphisms in DNA repair genes, traffic-related polycylic aromatic hydrocarbon exposure and breast cancer incidence
Vehicular traffic polycyclic aromatic hydrocarbons (PAHs) have been associated with breast cancer incidence in epidemiologic studies, including our own. Because PAHs damage DNA by forming adducts and oxidative lesions, genetic polymorphisms that alter DNA repair capacity may modify associations betw...
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Veröffentlicht in: | International journal of cancer 2016-04, Vol.139 (2), p.310-321 |
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creator | Mordukhovich, Irina Beyea, Jan Herring, Amy H. Hatch, Maureen Stellman, Steven D. Teitelbaum, Susan L. Richardson, David B. Millikan, Robert C. Engel, Lawrence S. Shantakumar, Sumitra Steck, Susan E. Neugut, Alfred I. Rossner, Pavel Santella, Regina M. Gammon, Marilie D. |
description | Vehicular traffic polycyclic aromatic hydrocarbons (PAHs) have been associated with breast cancer incidence in epidemiologic studies, including our own. Because PAHs damage DNA by forming adducts and oxidative lesions, genetic polymorphisms that alter DNA repair capacity may modify associations between PAH-related exposures and breast cancer risk. Our goal was to examine the association between vehicular traffic exposure and breast cancer incidence within strata of a panel of nine biologically plausible nucleotide excision repair (NER) and base excision repair (BER) genotypes. Residential histories of 1,508 cases and 1,556 controls were assessed in the Long Island Breast Cancer Study Project between 1996 and 1997 and used to reconstruct residential traffic exposures to benzo[a]pyrene, as a proxy for traffic-related PAHs. Likelihood ratio tests from adjusted unconditional logistic regression models were used to assess multiplicative interactions. A gene-traffic interaction was evident (
p
= 0.04) for
ERCC2
(Lys751); when comparing the upper and lower tertiles of 1995 traffic exposure estimates, the odds ratio (95% confidence interval) was 2.09 (1.13, 3.90) among women with homozygous variant alleles. Corresponding odds ratios for 1960–1990 traffic were also elevated nearly 2–3-fold for
XRCC1
(Arg194Trp),
XRCC1
(Arg399Gln) and
OGG1
(-Ser326Cys), but formal multiplicative interaction was not evident. When DNA repair variants for
ERCC2, XRCC1
and
OGG1
were combined, among women with 4–6 variants, the odds ratios were 2.32 (1.22, 4.49) for 1995 traffic and 2.96 (1.06, 8.21) for 1960–1990 traffic. Our study is first to report positive associations between traffic-related PAH exposure and breast cancer incidence among women with select biologically plausible DNA repair genotypes. |
doi_str_mv | 10.1002/ijc.30079 |
format | Article |
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p
= 0.04) for
ERCC2
(Lys751); when comparing the upper and lower tertiles of 1995 traffic exposure estimates, the odds ratio (95% confidence interval) was 2.09 (1.13, 3.90) among women with homozygous variant alleles. Corresponding odds ratios for 1960–1990 traffic were also elevated nearly 2–3-fold for
XRCC1
(Arg194Trp),
XRCC1
(Arg399Gln) and
OGG1
(-Ser326Cys), but formal multiplicative interaction was not evident. When DNA repair variants for
ERCC2, XRCC1
and
OGG1
were combined, among women with 4–6 variants, the odds ratios were 2.32 (1.22, 4.49) for 1995 traffic and 2.96 (1.06, 8.21) for 1960–1990 traffic. Our study is first to report positive associations between traffic-related PAH exposure and breast cancer incidence among women with select biologically plausible DNA repair genotypes.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.30079</identifier><identifier>PMID: 26946191</identifier><language>eng</language><ispartof>International journal of cancer, 2016-04, Vol.139 (2), p.310-321</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids></links><search><creatorcontrib>Mordukhovich, Irina</creatorcontrib><creatorcontrib>Beyea, Jan</creatorcontrib><creatorcontrib>Herring, Amy H.</creatorcontrib><creatorcontrib>Hatch, Maureen</creatorcontrib><creatorcontrib>Stellman, Steven D.</creatorcontrib><creatorcontrib>Teitelbaum, Susan L.</creatorcontrib><creatorcontrib>Richardson, David B.</creatorcontrib><creatorcontrib>Millikan, Robert C.</creatorcontrib><creatorcontrib>Engel, Lawrence S.</creatorcontrib><creatorcontrib>Shantakumar, Sumitra</creatorcontrib><creatorcontrib>Steck, Susan E.</creatorcontrib><creatorcontrib>Neugut, Alfred I.</creatorcontrib><creatorcontrib>Rossner, Pavel</creatorcontrib><creatorcontrib>Santella, Regina M.</creatorcontrib><creatorcontrib>Gammon, Marilie D.</creatorcontrib><title>Polymorphisms in DNA repair genes, traffic-related polycylic aromatic hydrocarbon exposure and breast cancer incidence</title><title>International journal of cancer</title><description>Vehicular traffic polycyclic aromatic hydrocarbons (PAHs) have been associated with breast cancer incidence in epidemiologic studies, including our own. Because PAHs damage DNA by forming adducts and oxidative lesions, genetic polymorphisms that alter DNA repair capacity may modify associations between PAH-related exposures and breast cancer risk. Our goal was to examine the association between vehicular traffic exposure and breast cancer incidence within strata of a panel of nine biologically plausible nucleotide excision repair (NER) and base excision repair (BER) genotypes. Residential histories of 1,508 cases and 1,556 controls were assessed in the Long Island Breast Cancer Study Project between 1996 and 1997 and used to reconstruct residential traffic exposures to benzo[a]pyrene, as a proxy for traffic-related PAHs. Likelihood ratio tests from adjusted unconditional logistic regression models were used to assess multiplicative interactions. A gene-traffic interaction was evident (
p
= 0.04) for
ERCC2
(Lys751); when comparing the upper and lower tertiles of 1995 traffic exposure estimates, the odds ratio (95% confidence interval) was 2.09 (1.13, 3.90) among women with homozygous variant alleles. Corresponding odds ratios for 1960–1990 traffic were also elevated nearly 2–3-fold for
XRCC1
(Arg194Trp),
XRCC1
(Arg399Gln) and
OGG1
(-Ser326Cys), but formal multiplicative interaction was not evident. When DNA repair variants for
ERCC2, XRCC1
and
OGG1
were combined, among women with 4–6 variants, the odds ratios were 2.32 (1.22, 4.49) for 1995 traffic and 2.96 (1.06, 8.21) for 1960–1990 traffic. Our study is first to report positive associations between traffic-related PAH exposure and breast cancer incidence among women with select biologically plausible DNA repair genotypes.</description><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqljbFOwzAURS0Eoikw8Af-AFKekyYhCxKCIibUgT16cV4aV4ltPacV-Xs8sDAz3SNd3XOFuFewUQDZoznqTQ5Q1RciUVBXKWSquBRJ7CCtVF6uxDqEI4BSBWyvxSor622papWI896Ny-TYDyZMQRor3z5fJJNHw_JAlsKDnBn73uiUacSZOunjRC-j0RLZTThHGJaOnUZunZX07V04MUm0nWyZMMxSo9XEUa9NRxFvxVWPY6C737wRz--7r9eP1J_aiTpNNp6OjWczIS-NQ9P8bawZmoM7N0VWF09Fnv9b8AODBGvs</recordid><startdate>20160406</startdate><enddate>20160406</enddate><creator>Mordukhovich, Irina</creator><creator>Beyea, Jan</creator><creator>Herring, Amy H.</creator><creator>Hatch, Maureen</creator><creator>Stellman, Steven D.</creator><creator>Teitelbaum, Susan L.</creator><creator>Richardson, David B.</creator><creator>Millikan, Robert C.</creator><creator>Engel, Lawrence S.</creator><creator>Shantakumar, Sumitra</creator><creator>Steck, Susan E.</creator><creator>Neugut, Alfred I.</creator><creator>Rossner, Pavel</creator><creator>Santella, Regina M.</creator><creator>Gammon, Marilie D.</creator><scope>5PM</scope></search><sort><creationdate>20160406</creationdate><title>Polymorphisms in DNA repair genes, traffic-related polycylic aromatic hydrocarbon exposure and breast cancer incidence</title><author>Mordukhovich, Irina ; Beyea, Jan ; Herring, Amy H. ; Hatch, Maureen ; Stellman, Steven D. ; Teitelbaum, Susan L. ; Richardson, David B. ; Millikan, Robert C. ; Engel, Lawrence S. ; Shantakumar, Sumitra ; Steck, Susan E. ; Neugut, Alfred I. ; Rossner, Pavel ; Santella, Regina M. ; Gammon, Marilie D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_52958533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mordukhovich, Irina</creatorcontrib><creatorcontrib>Beyea, Jan</creatorcontrib><creatorcontrib>Herring, Amy H.</creatorcontrib><creatorcontrib>Hatch, Maureen</creatorcontrib><creatorcontrib>Stellman, Steven D.</creatorcontrib><creatorcontrib>Teitelbaum, Susan L.</creatorcontrib><creatorcontrib>Richardson, David B.</creatorcontrib><creatorcontrib>Millikan, Robert C.</creatorcontrib><creatorcontrib>Engel, Lawrence S.</creatorcontrib><creatorcontrib>Shantakumar, Sumitra</creatorcontrib><creatorcontrib>Steck, Susan E.</creatorcontrib><creatorcontrib>Neugut, Alfred I.</creatorcontrib><creatorcontrib>Rossner, Pavel</creatorcontrib><creatorcontrib>Santella, Regina M.</creatorcontrib><creatorcontrib>Gammon, Marilie D.</creatorcontrib><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mordukhovich, Irina</au><au>Beyea, Jan</au><au>Herring, Amy H.</au><au>Hatch, Maureen</au><au>Stellman, Steven D.</au><au>Teitelbaum, Susan L.</au><au>Richardson, David B.</au><au>Millikan, Robert C.</au><au>Engel, Lawrence S.</au><au>Shantakumar, Sumitra</au><au>Steck, Susan E.</au><au>Neugut, Alfred I.</au><au>Rossner, Pavel</au><au>Santella, Regina M.</au><au>Gammon, Marilie D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polymorphisms in DNA repair genes, traffic-related polycylic aromatic hydrocarbon exposure and breast cancer incidence</atitle><jtitle>International journal of cancer</jtitle><date>2016-04-06</date><risdate>2016</risdate><volume>139</volume><issue>2</issue><spage>310</spage><epage>321</epage><pages>310-321</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><abstract>Vehicular traffic polycyclic aromatic hydrocarbons (PAHs) have been associated with breast cancer incidence in epidemiologic studies, including our own. Because PAHs damage DNA by forming adducts and oxidative lesions, genetic polymorphisms that alter DNA repair capacity may modify associations between PAH-related exposures and breast cancer risk. Our goal was to examine the association between vehicular traffic exposure and breast cancer incidence within strata of a panel of nine biologically plausible nucleotide excision repair (NER) and base excision repair (BER) genotypes. Residential histories of 1,508 cases and 1,556 controls were assessed in the Long Island Breast Cancer Study Project between 1996 and 1997 and used to reconstruct residential traffic exposures to benzo[a]pyrene, as a proxy for traffic-related PAHs. Likelihood ratio tests from adjusted unconditional logistic regression models were used to assess multiplicative interactions. A gene-traffic interaction was evident (
p
= 0.04) for
ERCC2
(Lys751); when comparing the upper and lower tertiles of 1995 traffic exposure estimates, the odds ratio (95% confidence interval) was 2.09 (1.13, 3.90) among women with homozygous variant alleles. Corresponding odds ratios for 1960–1990 traffic were also elevated nearly 2–3-fold for
XRCC1
(Arg194Trp),
XRCC1
(Arg399Gln) and
OGG1
(-Ser326Cys), but formal multiplicative interaction was not evident. When DNA repair variants for
ERCC2, XRCC1
and
OGG1
were combined, among women with 4–6 variants, the odds ratios were 2.32 (1.22, 4.49) for 1995 traffic and 2.96 (1.06, 8.21) for 1960–1990 traffic. Our study is first to report positive associations between traffic-related PAH exposure and breast cancer incidence among women with select biologically plausible DNA repair genotypes.</abstract><pmid>26946191</pmid><doi>10.1002/ijc.30079</doi></addata></record> |
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title | Polymorphisms in DNA repair genes, traffic-related polycylic aromatic hydrocarbon exposure and breast cancer incidence |
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