Common Variants in Immune and DNA Repair Genes and Risk for Human Papillomavirus Persistence and Progression to Cervical Cancer
Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer. Methods. We genotyped 92 single-nucleotide polymorphisms (SN...
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| Published in | The Journal of infectious diseases Vol. 199; no. 1; pp. 20 - 30 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
The University of Chicago Press
01.01.2009
University of Chicago Press Oxford University Press |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-1899 1537-6613 |
| DOI | 10.1086/595563 |
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| Abstract | Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer. Methods. We genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects. Results. A SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95–1.8-fold) and 1.7-fold (95% CI, 1.1–2.6-fold) increased risk for CIN3 or cancer, respectively (Ptrend=.008; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence (Ptrend=.009). Conclusions. Our results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence. |
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| AbstractList | We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer.
We genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects.
A SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95-1.8-fold) and 1.7-fold (95% CI, 1.1-2.6-fold) increased risk for CIN3 or cancer, respectively (P(trend) = .008; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence (P(trend) = .009).
Our results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence. Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer. Methods. We genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects. Results. A SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95–1.8-fold) and 1.7-fold (95% CI, 1.1–2.6–fold) increased risk for CIN3 or cancer, respectively ( $P_{trend} \, = .008$ ; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence ( $P_{trend} \, = .009$ . Conclusions. Our results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence. Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer. Methods. We genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects. Results. A SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95-1.8-fold) and 1.7-fold (95% CI, 1.1-2.6-fold) increased risk for CIN3 or cancer, respectively (P trend=.008; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence (P trend=.009). Conclusions. Our results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence. Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer. Methods. We genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects. Results. A SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95–1.8-fold) and 1.7-fold (95% CI, 1.1–2.6-fold) increased risk for CIN3 or cancer, respectively (Ptrend=.008; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence (Ptrend=.009). Conclusions. Our results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence. Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer. Methods. We genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects. Results. A SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95-1.8-fold) and 1.7-fold (95% CI, 1.1-2.6-fold) increased risk for CIN3 or cancer, respectively ([image] ; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence. Conclusions. Our results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer.BACKGROUNDWe examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and progress to cervical intraepithelial neoplasia grade 3 (CIN3) and cancer.We genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects.METHODSWe genotyped 92 single-nucleotide polymorphisms (SNPs) from 49 candidate immune response and DNA repair genes obtained from 469 women with CIN3 or cancer, 390 women with persistent HPV infections (median duration, 25 months), and 452 random control subjects from the 10,049-woman Guanacaste Costa Rica Natural History Study. We calculated odds ratios and 95% confidence intervals (CIs) for the association of SNP and haplotypes in women with CIN3 or cancer and HPV persistence, compared with random control subjects.A SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95-1.8-fold) and 1.7-fold (95% CI, 1.1-2.6-fold) increased risk for CIN3 or cancer, respectively (P(trend) = .008; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence (P(trend) = .009).RESULTSA SNP in the Fanconi anemia complementation group A gene (FANCA) (G501S) was associated with increased risk of CIN3 or cancer. The AG and GG genotypes had a 1.3-fold (95% CI, 0.95-1.8-fold) and 1.7-fold (95% CI, 1.1-2.6-fold) increased risk for CIN3 or cancer, respectively (P(trend) = .008; referent, AA). The FANCA haplotype that included G501S also conferred increased risk of CIN3 or cancer, as did a different haplotype that included 2 other FANCA SNPs (G809A and T266A). A SNP in the innate immune gene IRF3 (S427T) was associated with increased risk for HPV persistence (P(trend) = .009).Our results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence.CONCLUSIONSOur results require replication but support the role of FANCA variants in cervical cancer susceptibility and of IRF3 in HPV persistence. |
| Author | Porras, Carolina Wacholder, Sholom Burk, Robert D. Herrero, Rolando Lan, Z. Elizabeth Hildesheim, Allan Schiffman, Mark Wang, Sophia S. Chanock, Stephen J. Bratti, M. Concepcion Rodríguez, Ana Cecilia Sherman, Mark E. González, Paula |
| AuthorAffiliation | 1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 2 Core Genotyping Facility, National Cancer Institute, Gaithersburg, Maryland 4 Proyecto Epidemiológico Guanacaste, Fundación Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud, San José, Costa Rica 3 Albert Einstein School of Medicine, New York, New York |
| AuthorAffiliation_xml | – name: 3 Albert Einstein School of Medicine, New York, New York – name: 1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland – name: 4 Proyecto Epidemiológico Guanacaste, Fundación Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud, San José, Costa Rica – name: 2 Core Genotyping Facility, National Cancer Institute, Gaithersburg, Maryland |
| Author_xml | – sequence: 1 givenname: Sophia S. surname: Wang fullname: Wang, Sophia S. email: wangso@mail.nih.gov organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville – sequence: 2 givenname: M. Concepcion surname: Bratti fullname: Bratti, M. Concepcion organization: Proyecto Epidemiológico Guanacaste, Fundación Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud, San José, Costa Rica – sequence: 3 givenname: Ana Cecilia surname: Rodríguez fullname: Rodríguez, Ana Cecilia organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville – sequence: 4 givenname: Rolando surname: Herrero fullname: Herrero, Rolando organization: Proyecto Epidemiológico Guanacaste, Fundación Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud, San José, Costa Rica – sequence: 5 givenname: Robert D. surname: Burk fullname: Burk, Robert D. organization: Albert Einstein School of Medicine, New York, New York – sequence: 6 givenname: Carolina surname: Porras fullname: Porras, Carolina organization: Proyecto Epidemiológico Guanacaste, Fundación Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud, San José, Costa Rica – sequence: 7 givenname: Paula surname: González fullname: González, Paula organization: Proyecto Epidemiológico Guanacaste, Fundación Instituto Costarricense de Investigación y Enseñanza en Nutrición y Salud, San José, Costa Rica – sequence: 8 givenname: Mark E. surname: Sherman fullname: Sherman, Mark E. organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville – sequence: 9 givenname: Sholom surname: Wacholder fullname: Wacholder, Sholom organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville – sequence: 10 givenname: Z. Elizabeth surname: Lan fullname: Lan, Z. Elizabeth organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville – sequence: 11 givenname: Mark surname: Schiffman fullname: Schiffman, Mark organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville – sequence: 12 givenname: Stephen J. surname: Chanock fullname: Chanock, Stephen J. organization: Core Genotyping Facility, National Cancer Institute, Gaithersburg, Maryland – sequence: 13 givenname: Allan surname: Hildesheim fullname: Hildesheim, Allan organization: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville |
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| Copyright | Copyright 2008 Infectious Diseases Society of America 2009 by the Infectious Diseases Society of America 2009 2009 INIST-CNRS 2008 by the Infectious Diseases Society of America. All rights reserved. 2008 |
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| Keywords | Microbiology Papovaviridae Malignant tumor Female genital diseases Papillomavirus Virus Infection Human papillomavirus Gene Repair Uterine cervix diseases Cervical cancer Cancer |
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| References_xml | – volume: 11 start-page: 1513 year: 2002 ident: 2016042623535343000_199.1.20.32 article-title: Polymorphisms in DNA repair genes and associations with cancer risk publication-title: Cancer Epidemiol Biomarkers Prev – ident: 2016042623535343000_199.1.20.35 doi: 10.1038/sj.cr.7290309 – ident: 2016042623535343000_199.1.20.6 doi: 10.1016/j.ijgo.2003.08.017 – ident: 2016042623535343000_199.1.20.1 doi: 10.1016/S1470-2045(05)70086-3 – volume: 20 start-page: 731 year: 2007 ident: 2016042623535343000_199.1.20.8 article-title: Is the p53 codon 72 polymorphism a key biomarker for cervical cancer development? A meta-analysis review within European populations publication-title: Int J Mol Med – ident: 2016042623535343000_199.1.20.15 doi: 10.1111/j.1525-1438.2005.00433.x – ident: 2016042623535343000_199.1.20.18 doi: 10.1001/jama.283.1.87 – volume: 12 start-page: 921 year: 1995 ident: 2016042623535343000_199.1.20.24 article-title: Maximum-likelihood estimation of molecular haplotype frequencies in a diploid population publication-title: Mol Biol Evol – ident: 2016042623535343000_199.1.20.7 doi: 10.1158/1055-9965.EPI-083-3 – ident: 2016042623535343000_199.1.20.38 doi: 10.1074/jbc.M510182200 – ident: 2016042623535343000_199.1.20.39 doi: 10.1128/IAI.72.10.5799-5806.2004 – ident: 2016042623535343000_199.1.20.2 doi: 10.1016/j.vaccine.2006.05.115 – ident: 2016042623535343000_199.1.20.23 doi: 10.1093/bioinformatics/bth457 – volume: 114 start-page: 173 year: 2008 ident: 2016042623535343000_199.1.20.30 article-title: NADPH oxidase CYBA polymorphisms, oxidative stress and cardiovascular diseases publication-title: Clin Sci (Lond) doi: 10.1042/CS20070130 – ident: 2016042623535343000_199.1.20.16 doi: 10.1093/jnci/92.6.464 – ident: 2016042623535343000_199.1.20.28 doi: 10.1038/nrc970 – ident: 2016042623535343000_199.1.20.11 doi: 10.1002/ijc.1543 – ident: 2016042623535343000_199.1.20.22 doi: 10.1093/jnci/djh075 – ident: 2016042623535343000_199.1.20.3 doi: 10.1002/1097-0215(20001201)88:5<698::AID-IJC3>3.0.CO;2-J – ident: 2016042623535343000_199.1.20.37 doi: 10.1038/sj.cr.7310019 – ident: 2016042623535343000_199.1.20.26 doi: 10.1086/338688 – ident: 2016042623535343000_199.1.20.14 doi: 10.1158/0008-5472.CAN-07-2677 – ident: 2016042623535343000_199.1.20.10 doi: 10.1002/ijc.22989 – ident: 2016042623535343000_199.1.20.12 doi: 10.1046/j.1365-2370.2002.00347.x – ident: 2016042623535343000_199.1.20.25 – ident: 2016042623535343000_199.1.20.27 doi: 10.1002/em.20109 – ident: 2016042623535343000_199.1.20.19 doi: 10.1086/428850 – ident: 2016042623535343000_199.1.20.4 doi: 10.1016/S0168-1702(02)00191-0 – ident: 2016042623535343000_199.1.20.5 doi: 10.1093/oxfordjournals.jncimonographs.a003480 – volume: 1 start-page: 362 year: 1997 ident: 2016042623535343000_199.1.20.17 article-title: Design and methods of a population-based natural history study of cervical neoplasia in a rural province of Costa Rica: the Guanacaste Project publication-title: Rev Panam Salud Publica doi: 10.1590/S1020-49891997000500005 – ident: 2016042623535343000_199.1.20.20 doi: 10.1093/nar/gkj151 – volume: 111 start-page: 1843 year: 2003 ident: 2016042623535343000_199.1.20.34 article-title: Functional characterization of polymorphisms in DNA repair genes using cytogenetic challenge assays publication-title: Environ Health Perspect doi: 10.1289/ehp.6632 – volume: 12 start-page: 1100 year: 2003 ident: 2016042623535343000_199.1.20.33 article-title: Nasopharyngeal carcinoma and genetic polymorphisms of DNA repair enzymes XRCC1 and hOGG1 publication-title: Cancer Epidemiol Biomarkers Prev – ident: 2016042623535343000_199.1.20.13 doi: 10.1089/107999004323034114 – volume: 13 start-page: 2446 year: 2007 ident: 2016042623535343000_199.1.20.36 article-title: The interferon inducing pathways and the hepatitis C virus publication-title: World J Gastroenterol doi: 10.3748/wjg.v13.i17.2446 – ident: 2016042623535343000_199.1.20.9 doi: 10.1086/427826 – volume: 2 start-page: 427 year: 2004 ident: 2016042623535343000_199.1.20.29 article-title: Is hEXO1 a cancer predisposing gene? publication-title: Mol Cancer Res doi: 10.1158/1541-7786.427.2.8 – volume: 18 start-page: 955 year: 2003 ident: 2016042623535343000_199.1.20.31 article-title: XRCC1 and DNA strand break repair publication-title: DNA Repair (Amst) doi: 10.1016/S1568-7864(03)00118-6 – volume: 57 start-page: 289 year: 1995 ident: 2016042623535343000_199.1.20.21 article-title: Controlling the false discovery rate: a practical and powerful approach to multiple testing publication-title: J Roy Stat Soc B doi: 10.1111/j.2517-6161.1995.tb02031.x |
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| Snippet | Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to... Background. We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to... We examined host genetic factors to identify those more common in individuals whose human papillomavirus (HPV) infections were most likely to persist and... |
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| SubjectTerms | Biological and medical sciences Cancer Cervical cancer Cohort Studies Costa Rica - epidemiology Disease Progression DNA Probes, HPV DNA repair DNA Repair - genetics DNA, Viral - isolation & purification DNA-Binding Proteins - genetics Exodeoxyribonucleases - genetics Fanconi Anemia Complementation Group A Protein - genetics Female Fundamental and applied biological sciences. Psychology Genes, BRCA1 Genes, BRCA2 Genetic polymorphism Genotypes Haplotypes Human genetics Human papillomavirus Humans Immune response Infections Infectious diseases Medical genetics Medical sciences Microbiology Miscellaneous NADPH Oxidases - genetics Papillomaviridae - isolation & purification Papillomavirus Infections - complications Papillomavirus Infections - epidemiology Papillomavirus Infections - physiopathology Polymorphism, Single Nucleotide Tumors Uterine Cervical Neoplasms - epidemiology Uterine Cervical Neoplasms - genetics Virology Viruses X-ray Repair Cross Complementing Protein 1 |
| Title | Common Variants in Immune and DNA Repair Genes and Risk for Human Papillomavirus Persistence and Progression to Cervical Cancer |
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