Polymorphisms in XRCC1 Modify the Association between Polycyclic Aromatic Hydrocarbon-DNA Adducts, Cigarette Smoking, Dietary Antioxidants, and Breast Cancer Risk
The variability in DNA repair capacity of the general population may depend in part upon common variants in DNA repair genes. X-ray repair cross complementing group 1 ( XRCC1 ) is an important DNA base excision repair gene and exhibits polymorphic variation. Using the Long Island Breast Cancer Study...
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| creator | JING SHEN GAMMON, Marilie D NEUGUT, Alfred I SANTELLA, Regina M TERRY, Mary Beth LIANWEN WANG QIAO WANG FANGFANG ZHANG TEITELBAUM, Susan L ENG, Sybil M SAGIV, Sharon K GAUDET, Mia M |
| description | The variability in DNA repair capacity of the general population may depend in part upon common variants in DNA repair genes.
X-ray repair cross complementing group 1 ( XRCC1 ) is an important DNA base excision repair gene and exhibits polymorphic variation. Using the Long Island Breast Cancer Study
Project, a population-based case-control study, we evaluated the hypothesis that two common single nucleotide polymorphisms
of XRCC1 (codon 194 Arg→Trp and 399 Arg→Gln) influence breast cancer susceptibility and interact with polycyclic aromatic hydrocarbon
(PAH)-DNA adducts, cigarette smoking, and intake of fruits and vegetables and antioxidants. The available sample for genotyping
included 1,067 cases and 1,110 controls. Genotyping was done by a high-throughput single-nucleotide extension assay with fluorescence
polarization detection of the incorporated nucleotide. We observed no significant increases in risk among all subjects who
were carriers of XRCC1 194Trp or 399Gln alleles. Among never smokers, we observed an increased risk of breast cancer in 399Gln carriers [odds ratio
(OR), 1.3; 95% confidence interval (CI), 1.0-1.7). Further analysis indicated a suggestive weak additive interaction between
the 399Gln allele and detectable PAH-DNA adducts (OR for exposure with mutant genotype, 1.9; 95% CI, 1.2-3.1). The estimated
age-adjusted interaction contrast ratio (ICR) and 95% CI (ICR, 0.38; 95% CI, −0.32 to 1.10) indicated that the departure from
additivity was not statistically significant, but that there was some suggestion of a relative excess risk due to the interaction.
In subjects with at least one copy of XRCC1 194Trp allele, there was a moderate interaction with high intake of fruits and vegetables (≥35 half-cup servings per week
of any fruits, fruit juices, and vegetables, OR, 0.58; 95% CI, 0.38-0.89; ICR, −0.49; 95% CI, −0.03 to −0.95), and dietary
plus supplement antioxidant intake with 33% to 42% decreases in breast cancer risk compared with those with the Arg194Arg
genotype and low-intake individuals. These results do not show that the two genetic polymorphisms of XRCC1 independently influence breast cancer risk. However, there is evidence for interactions between the two XRCC1 single nucleotide polymorphisms and PAH-DNA adducts or fruit and vegetable and antioxidant intake on breast cancer risk.
Further understanding of the biological function of XRCC1 variants and their interactions with PAH-DNA adducts, antioxidants, and other genes in the pat |
| doi_str_mv | 10.1158/1055-9965.EPI-04-0414 |
| format | Article |
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X-ray repair cross complementing group 1 ( XRCC1 ) is an important DNA base excision repair gene and exhibits polymorphic variation. Using the Long Island Breast Cancer Study
Project, a population-based case-control study, we evaluated the hypothesis that two common single nucleotide polymorphisms
of XRCC1 (codon 194 Arg→Trp and 399 Arg→Gln) influence breast cancer susceptibility and interact with polycyclic aromatic hydrocarbon
(PAH)-DNA adducts, cigarette smoking, and intake of fruits and vegetables and antioxidants. The available sample for genotyping
included 1,067 cases and 1,110 controls. Genotyping was done by a high-throughput single-nucleotide extension assay with fluorescence
polarization detection of the incorporated nucleotide. We observed no significant increases in risk among all subjects who
were carriers of XRCC1 194Trp or 399Gln alleles. Among never smokers, we observed an increased risk of breast cancer in 399Gln carriers [odds ratio
(OR), 1.3; 95% confidence interval (CI), 1.0-1.7). Further analysis indicated a suggestive weak additive interaction between
the 399Gln allele and detectable PAH-DNA adducts (OR for exposure with mutant genotype, 1.9; 95% CI, 1.2-3.1). The estimated
age-adjusted interaction contrast ratio (ICR) and 95% CI (ICR, 0.38; 95% CI, −0.32 to 1.10) indicated that the departure from
additivity was not statistically significant, but that there was some suggestion of a relative excess risk due to the interaction.
In subjects with at least one copy of XRCC1 194Trp allele, there was a moderate interaction with high intake of fruits and vegetables (≥35 half-cup servings per week
of any fruits, fruit juices, and vegetables, OR, 0.58; 95% CI, 0.38-0.89; ICR, −0.49; 95% CI, −0.03 to −0.95), and dietary
plus supplement antioxidant intake with 33% to 42% decreases in breast cancer risk compared with those with the Arg194Arg
genotype and low-intake individuals. These results do not show that the two genetic polymorphisms of XRCC1 independently influence breast cancer risk. However, there is evidence for interactions between the two XRCC1 single nucleotide polymorphisms and PAH-DNA adducts or fruit and vegetable and antioxidant intake on breast cancer risk.
Further understanding of the biological function of XRCC1 variants and their interactions with PAH-DNA adducts, antioxidants, and other genes in the pathway are needed.</description><identifier>ISSN: 1055-9965</identifier><identifier>EISSN: 1538-7755</identifier><identifier>DOI: 10.1158/1055-9965.EPI-04-0414</identifier><identifier>PMID: 15734955</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adult ; Antioxidants ; Antioxidants - metabolism ; Biological and medical sciences ; Breast Cancer Risk ; Breast Neoplasms - epidemiology ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Case-Control Studies ; Diet ; Dietary Supplements ; DNA Adducts - metabolism ; DNA-Binding Proteins - genetics ; Female ; Genotype ; Gynecology. Andrology. Obstetrics ; Humans ; Long Island ; Mammary gland diseases ; Medical sciences ; Middle Aged ; PAH-DNA adducts ; Polycyclic Aromatic Hydrocarbons - metabolism ; Polymorphism, Single Nucleotide ; Risk Factors ; Smoking - physiopathology ; Tumors ; X-ray Repair Cross Complementing Protein 1 ; XRCC1</subject><ispartof>Cancer epidemiology, biomarkers & prevention, 2005-02, Vol.14 (2), p.336-342</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-f8122ba94455da42aee4f6a22ffa8acb619e8adcef5a61ad5a13df01c3e334ce3</citedby><cites>FETCH-LOGICAL-c466t-f8122ba94455da42aee4f6a22ffa8acb619e8adcef5a61ad5a13df01c3e334ce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16556324$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15734955$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JING SHEN</creatorcontrib><creatorcontrib>GAMMON, Marilie D</creatorcontrib><creatorcontrib>NEUGUT, Alfred I</creatorcontrib><creatorcontrib>SANTELLA, Regina M</creatorcontrib><creatorcontrib>TERRY, Mary Beth</creatorcontrib><creatorcontrib>LIANWEN WANG</creatorcontrib><creatorcontrib>QIAO WANG</creatorcontrib><creatorcontrib>FANGFANG ZHANG</creatorcontrib><creatorcontrib>TEITELBAUM, Susan L</creatorcontrib><creatorcontrib>ENG, Sybil M</creatorcontrib><creatorcontrib>SAGIV, Sharon K</creatorcontrib><creatorcontrib>GAUDET, Mia M</creatorcontrib><title>Polymorphisms in XRCC1 Modify the Association between Polycyclic Aromatic Hydrocarbon-DNA Adducts, Cigarette Smoking, Dietary Antioxidants, and Breast Cancer Risk</title><title>Cancer epidemiology, biomarkers & prevention</title><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><description>The variability in DNA repair capacity of the general population may depend in part upon common variants in DNA repair genes.
X-ray repair cross complementing group 1 ( XRCC1 ) is an important DNA base excision repair gene and exhibits polymorphic variation. Using the Long Island Breast Cancer Study
Project, a population-based case-control study, we evaluated the hypothesis that two common single nucleotide polymorphisms
of XRCC1 (codon 194 Arg→Trp and 399 Arg→Gln) influence breast cancer susceptibility and interact with polycyclic aromatic hydrocarbon
(PAH)-DNA adducts, cigarette smoking, and intake of fruits and vegetables and antioxidants. The available sample for genotyping
included 1,067 cases and 1,110 controls. Genotyping was done by a high-throughput single-nucleotide extension assay with fluorescence
polarization detection of the incorporated nucleotide. We observed no significant increases in risk among all subjects who
were carriers of XRCC1 194Trp or 399Gln alleles. Among never smokers, we observed an increased risk of breast cancer in 399Gln carriers [odds ratio
(OR), 1.3; 95% confidence interval (CI), 1.0-1.7). Further analysis indicated a suggestive weak additive interaction between
the 399Gln allele and detectable PAH-DNA adducts (OR for exposure with mutant genotype, 1.9; 95% CI, 1.2-3.1). The estimated
age-adjusted interaction contrast ratio (ICR) and 95% CI (ICR, 0.38; 95% CI, −0.32 to 1.10) indicated that the departure from
additivity was not statistically significant, but that there was some suggestion of a relative excess risk due to the interaction.
In subjects with at least one copy of XRCC1 194Trp allele, there was a moderate interaction with high intake of fruits and vegetables (≥35 half-cup servings per week
of any fruits, fruit juices, and vegetables, OR, 0.58; 95% CI, 0.38-0.89; ICR, −0.49; 95% CI, −0.03 to −0.95), and dietary
plus supplement antioxidant intake with 33% to 42% decreases in breast cancer risk compared with those with the Arg194Arg
genotype and low-intake individuals. These results do not show that the two genetic polymorphisms of XRCC1 independently influence breast cancer risk. However, there is evidence for interactions between the two XRCC1 single nucleotide polymorphisms and PAH-DNA adducts or fruit and vegetable and antioxidant intake on breast cancer risk.
Further understanding of the biological function of XRCC1 variants and their interactions with PAH-DNA adducts, antioxidants, and other genes in the pathway are needed.</description><subject>Adult</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Biological and medical sciences</subject><subject>Breast Cancer Risk</subject><subject>Breast Neoplasms - epidemiology</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Case-Control Studies</subject><subject>Diet</subject><subject>Dietary Supplements</subject><subject>DNA Adducts - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Female</subject><subject>Genotype</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Long Island</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>PAH-DNA adducts</subject><subject>Polycyclic Aromatic Hydrocarbons - metabolism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Factors</subject><subject>Smoking - physiopathology</subject><subject>Tumors</subject><subject>X-ray Repair Cross Complementing Protein 1</subject><subject>XRCC1</subject><issn>1055-9965</issn><issn>1538-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQhyMEoqXwCCBfgEtT7PhPkmOatrRSgaqAxM2atSe7pkm82Fm1-zo8KQ67qEckSx7J329Gni_LXjN6wpisPjAqZV7XSp6c31zlVKTDxJPskEle5WUp5dNU_2MOshcx_qSUlrWUz7MDJksuUnmY_b7x_XbwYb1ycYjEjeTHbdsy8slb123JtELSxOiNg8n5kSxwukccyZwyW9M7Q5rgh_RoyOXWBm8gLPyYn31uSGPtxkzxmLRuCQGnCcnXwd-5cXlMzhxOELakGVPbB2dhnEEYLTkNCHEiLYwGA7l18e5l9qyDPuKr_X2Ufb84_9Ze5tdfPl61zXVuhFJT3lWsKBZQCyGlBVEAougUFEXXQQVmoViNFViDnQTFwEpg3HaUGY6cC4P8KHu367sO_tcG46QHFw32PYzoN1GrUihai-K_ICsryitWJlDuQBN8jAE7vQ5uSP_WjOrZop4N6dmQThY1FXq2mHJv9gM2iwHtY2qvLQFv9wBEA30X0rZcfOSUlIoXc6P3O27llqt7F1Cbv3sNGBGCWWkmdKE5V_wPmXS2MQ</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>JING SHEN</creator><creator>GAMMON, Marilie D</creator><creator>NEUGUT, Alfred I</creator><creator>SANTELLA, Regina M</creator><creator>TERRY, Mary Beth</creator><creator>LIANWEN WANG</creator><creator>QIAO WANG</creator><creator>FANGFANG ZHANG</creator><creator>TEITELBAUM, Susan L</creator><creator>ENG, Sybil M</creator><creator>SAGIV, Sharon K</creator><creator>GAUDET, Mia M</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20050201</creationdate><title>Polymorphisms in XRCC1 Modify the Association between Polycyclic Aromatic Hydrocarbon-DNA Adducts, Cigarette Smoking, Dietary Antioxidants, and Breast Cancer Risk</title><author>JING SHEN ; GAMMON, Marilie D ; NEUGUT, Alfred I ; SANTELLA, Regina M ; TERRY, Mary Beth ; LIANWEN WANG ; QIAO WANG ; FANGFANG ZHANG ; TEITELBAUM, Susan L ; ENG, Sybil M ; SAGIV, Sharon K ; GAUDET, Mia M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-f8122ba94455da42aee4f6a22ffa8acb619e8adcef5a61ad5a13df01c3e334ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>Biological and medical sciences</topic><topic>Breast Cancer Risk</topic><topic>Breast Neoplasms - epidemiology</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Case-Control Studies</topic><topic>Diet</topic><topic>Dietary Supplements</topic><topic>DNA Adducts - metabolism</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Female</topic><topic>Genotype</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Long Island</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>PAH-DNA adducts</topic><topic>Polycyclic Aromatic Hydrocarbons - metabolism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Risk Factors</topic><topic>Smoking - physiopathology</topic><topic>Tumors</topic><topic>X-ray Repair Cross Complementing Protein 1</topic><topic>XRCC1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>JING SHEN</creatorcontrib><creatorcontrib>GAMMON, Marilie D</creatorcontrib><creatorcontrib>NEUGUT, Alfred I</creatorcontrib><creatorcontrib>SANTELLA, Regina M</creatorcontrib><creatorcontrib>TERRY, Mary Beth</creatorcontrib><creatorcontrib>LIANWEN WANG</creatorcontrib><creatorcontrib>QIAO WANG</creatorcontrib><creatorcontrib>FANGFANG ZHANG</creatorcontrib><creatorcontrib>TEITELBAUM, Susan L</creatorcontrib><creatorcontrib>ENG, Sybil M</creatorcontrib><creatorcontrib>SAGIV, Sharon K</creatorcontrib><creatorcontrib>GAUDET, Mia M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JING SHEN</au><au>GAMMON, Marilie D</au><au>NEUGUT, Alfred I</au><au>SANTELLA, Regina M</au><au>TERRY, Mary Beth</au><au>LIANWEN WANG</au><au>QIAO WANG</au><au>FANGFANG ZHANG</au><au>TEITELBAUM, Susan L</au><au>ENG, Sybil M</au><au>SAGIV, Sharon K</au><au>GAUDET, Mia M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polymorphisms in XRCC1 Modify the Association between Polycyclic Aromatic Hydrocarbon-DNA Adducts, Cigarette Smoking, Dietary Antioxidants, and Breast Cancer Risk</atitle><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>14</volume><issue>2</issue><spage>336</spage><epage>342</epage><pages>336-342</pages><issn>1055-9965</issn><eissn>1538-7755</eissn><abstract>The variability in DNA repair capacity of the general population may depend in part upon common variants in DNA repair genes.
X-ray repair cross complementing group 1 ( XRCC1 ) is an important DNA base excision repair gene and exhibits polymorphic variation. Using the Long Island Breast Cancer Study
Project, a population-based case-control study, we evaluated the hypothesis that two common single nucleotide polymorphisms
of XRCC1 (codon 194 Arg→Trp and 399 Arg→Gln) influence breast cancer susceptibility and interact with polycyclic aromatic hydrocarbon
(PAH)-DNA adducts, cigarette smoking, and intake of fruits and vegetables and antioxidants. The available sample for genotyping
included 1,067 cases and 1,110 controls. Genotyping was done by a high-throughput single-nucleotide extension assay with fluorescence
polarization detection of the incorporated nucleotide. We observed no significant increases in risk among all subjects who
were carriers of XRCC1 194Trp or 399Gln alleles. Among never smokers, we observed an increased risk of breast cancer in 399Gln carriers [odds ratio
(OR), 1.3; 95% confidence interval (CI), 1.0-1.7). Further analysis indicated a suggestive weak additive interaction between
the 399Gln allele and detectable PAH-DNA adducts (OR for exposure with mutant genotype, 1.9; 95% CI, 1.2-3.1). The estimated
age-adjusted interaction contrast ratio (ICR) and 95% CI (ICR, 0.38; 95% CI, −0.32 to 1.10) indicated that the departure from
additivity was not statistically significant, but that there was some suggestion of a relative excess risk due to the interaction.
In subjects with at least one copy of XRCC1 194Trp allele, there was a moderate interaction with high intake of fruits and vegetables (≥35 half-cup servings per week
of any fruits, fruit juices, and vegetables, OR, 0.58; 95% CI, 0.38-0.89; ICR, −0.49; 95% CI, −0.03 to −0.95), and dietary
plus supplement antioxidant intake with 33% to 42% decreases in breast cancer risk compared with those with the Arg194Arg
genotype and low-intake individuals. These results do not show that the two genetic polymorphisms of XRCC1 independently influence breast cancer risk. However, there is evidence for interactions between the two XRCC1 single nucleotide polymorphisms and PAH-DNA adducts or fruit and vegetable and antioxidant intake on breast cancer risk.
Further understanding of the biological function of XRCC1 variants and their interactions with PAH-DNA adducts, antioxidants, and other genes in the pathway are needed.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>15734955</pmid><doi>10.1158/1055-9965.EPI-04-0414</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1055-9965 |
| ispartof | Cancer epidemiology, biomarkers & prevention, 2005-02, Vol.14 (2), p.336-342 |
| issn | 1055-9965 1538-7755 |
| language | eng |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Antioxidants Antioxidants - metabolism Biological and medical sciences Breast Cancer Risk Breast Neoplasms - epidemiology Breast Neoplasms - genetics Breast Neoplasms - metabolism Case-Control Studies Diet Dietary Supplements DNA Adducts - metabolism DNA-Binding Proteins - genetics Female Genotype Gynecology. Andrology. Obstetrics Humans Long Island Mammary gland diseases Medical sciences Middle Aged PAH-DNA adducts Polycyclic Aromatic Hydrocarbons - metabolism Polymorphism, Single Nucleotide Risk Factors Smoking - physiopathology Tumors X-ray Repair Cross Complementing Protein 1 XRCC1 |
| title | Polymorphisms in XRCC1 Modify the Association between Polycyclic Aromatic Hydrocarbon-DNA Adducts, Cigarette Smoking, Dietary Antioxidants, and Breast Cancer Risk |
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