Interaction between organochlorines and the AHR gene, and risk of non-Hodgkin lymphoma

Background Plasma organochlorines have been implicated to increase the risk of non-Hodgkin lymphoma (NHL), and interaction with the aryl hydrocarbon receptor gene (AHR) may modify this risk. Methods In this case-control study conducted in British Columbia, Canada, five single nucleotide polymorphism...

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Veröffentlicht in:Cancer causes & control 2010-01, Vol.21 (1), p.11-22
Hauptverfasser: Ng, Carmen H, Janoo-Gilani, Rozmin, Sipahimalani, Payal, Gallagher, Richard P, Gascoyne, Randy D, Connors, Joseph M, Weber, Jean-Philippe, Lai, Agnes S, Leach, Stephen, Le, Nhu D, Brooks-Wilson, Angela R, Spinelli, John J
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container_end_page 22
container_issue 1
container_start_page 11
container_title Cancer causes & control
container_volume 21
creator Ng, Carmen H
Janoo-Gilani, Rozmin
Sipahimalani, Payal
Gallagher, Richard P
Gascoyne, Randy D
Connors, Joseph M
Weber, Jean-Philippe
Lai, Agnes S
Leach, Stephen
Le, Nhu D
Brooks-Wilson, Angela R
Spinelli, John J
description Background Plasma organochlorines have been implicated to increase the risk of non-Hodgkin lymphoma (NHL), and interaction with the aryl hydrocarbon receptor gene (AHR) may modify this risk. Methods In this case-control study conducted in British Columbia, Canada, five single nucleotide polymorphisms (SNPs) of AHR were genotyped in 422 NHL cases and 459 controls to measure the association between individual SNPs, haplotypes, and risk of NHL. Pre-chemotherapy organochlorine levels were measured and gene-environment interaction analysis was performed. Results The IVS1 + 4640G/A SNP was significantly associated with NHL risk, with an odds ratio of 1.32 (95% CI = 1.05-1.65) for G/A or A/A genotypes compared to the G/G genotype. Interactions were observed with PCB 118, a known inducer of AHR, and chlordane-related analytes oxychlordane and trans-nonachlor, although no interactions were statistically significant after controlling for multiple comparisons. The observed interactions were consistent across NHL subtypes. Conclusion Results suggest that the AHR gene may play a role in determining the risk of NHL with exposure to organochlorines, and highlight the importance of understanding gene-environment interactions.
doi_str_mv 10.1007/s10552-009-9429-5
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Methods In this case-control study conducted in British Columbia, Canada, five single nucleotide polymorphisms (SNPs) of AHR were genotyped in 422 NHL cases and 459 controls to measure the association between individual SNPs, haplotypes, and risk of NHL. Pre-chemotherapy organochlorine levels were measured and gene-environment interaction analysis was performed. Results The IVS1 + 4640G/A SNP was significantly associated with NHL risk, with an odds ratio of 1.32 (95% CI = 1.05-1.65) for G/A or A/A genotypes compared to the G/G genotype. Interactions were observed with PCB 118, a known inducer of AHR, and chlordane-related analytes oxychlordane and trans-nonachlor, although no interactions were statistically significant after controlling for multiple comparisons. The observed interactions were consistent across NHL subtypes. Conclusion Results suggest that the AHR gene may play a role in determining the risk of NHL with exposure to organochlorines, and highlight the importance of understanding gene-environment interactions.</description><identifier>ISSN: 0957-5243</identifier><identifier>EISSN: 1573-7225</identifier><identifier>DOI: 10.1007/s10552-009-9429-5</identifier><identifier>PMID: 19821039</identifier><identifier>CODEN: CCCNEN</identifier><language>eng</language><publisher>Dordrecht: Dordrecht : Springer Netherlands</publisher><subject>Adult ; Aged ; Alleles ; Aryl hydrocarbon receptors ; Basic Helix-Loop-Helix Transcription Factors ; Biomedical and Life Sciences ; Biomedicine ; British Columbia ; Cancer ; Cancer Research ; Case-Control Studies ; Chemotherapy ; Dioxins ; Environmental Exposure ; Environmental Pollutants - blood ; Epidemiology ; Exons ; Genes ; Genetic Predisposition to Disease ; Genetic testing ; Genotype ; Genotypes ; Haplotypes ; Hematology ; Humans ; Hydrocarbons ; Hydrocarbons, Chlorinated - blood ; Kinases ; Lymphoma ; Lymphoma, Non-Hodgkin - epidemiology ; Lymphoma, Non-Hodgkin - genetics ; Middle Aged ; Non Hodgkin lymphoma ; Oncology ; Original Paper ; PCB ; Pesticides ; Plasma ; Polychlorinated biphenyls ; Polymorphism, Single Nucleotide ; Public Health ; Receptors, Aryl Hydrocarbon - genetics ; Risk Factors ; Sequencing ; T lymphocytes ; Toxicity</subject><ispartof>Cancer causes &amp; control, 2010-01, Vol.21 (1), p.11-22</ispartof><rights>Copyright 2010 Springer</rights><rights>Springer Science+Business Media B.V. 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-b2a93c83897087a9aa1596e42c456612be31a5ba5074671e8d06fbee766845b33</citedby><cites>FETCH-LOGICAL-c514t-b2a93c83897087a9aa1596e42c456612be31a5ba5074671e8d06fbee766845b33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25621323$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25621323$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,777,781,800,27905,27906,41469,42538,51300,57998,58231</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19821039$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ng, Carmen H</creatorcontrib><creatorcontrib>Janoo-Gilani, Rozmin</creatorcontrib><creatorcontrib>Sipahimalani, Payal</creatorcontrib><creatorcontrib>Gallagher, Richard P</creatorcontrib><creatorcontrib>Gascoyne, Randy D</creatorcontrib><creatorcontrib>Connors, Joseph M</creatorcontrib><creatorcontrib>Weber, Jean-Philippe</creatorcontrib><creatorcontrib>Lai, Agnes S</creatorcontrib><creatorcontrib>Leach, Stephen</creatorcontrib><creatorcontrib>Le, Nhu D</creatorcontrib><creatorcontrib>Brooks-Wilson, Angela R</creatorcontrib><creatorcontrib>Spinelli, John J</creatorcontrib><title>Interaction between organochlorines and the AHR gene, and risk of non-Hodgkin lymphoma</title><title>Cancer causes &amp; control</title><addtitle>Cancer Causes Control</addtitle><addtitle>Cancer Causes Control</addtitle><description>Background Plasma organochlorines have been implicated to increase the risk of non-Hodgkin lymphoma (NHL), and interaction with the aryl hydrocarbon receptor gene (AHR) may modify this risk. Methods In this case-control study conducted in British Columbia, Canada, five single nucleotide polymorphisms (SNPs) of AHR were genotyped in 422 NHL cases and 459 controls to measure the association between individual SNPs, haplotypes, and risk of NHL. Pre-chemotherapy organochlorine levels were measured and gene-environment interaction analysis was performed. Results The IVS1 + 4640G/A SNP was significantly associated with NHL risk, with an odds ratio of 1.32 (95% CI = 1.05-1.65) for G/A or A/A genotypes compared to the G/G genotype. Interactions were observed with PCB 118, a known inducer of AHR, and chlordane-related analytes oxychlordane and trans-nonachlor, although no interactions were statistically significant after controlling for multiple comparisons. The observed interactions were consistent across NHL subtypes. 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control</jtitle><stitle>Cancer Causes Control</stitle><addtitle>Cancer Causes Control</addtitle><date>2010-01-01</date><risdate>2010</risdate><volume>21</volume><issue>1</issue><spage>11</spage><epage>22</epage><pages>11-22</pages><issn>0957-5243</issn><eissn>1573-7225</eissn><coden>CCCNEN</coden><abstract>Background Plasma organochlorines have been implicated to increase the risk of non-Hodgkin lymphoma (NHL), and interaction with the aryl hydrocarbon receptor gene (AHR) may modify this risk. Methods In this case-control study conducted in British Columbia, Canada, five single nucleotide polymorphisms (SNPs) of AHR were genotyped in 422 NHL cases and 459 controls to measure the association between individual SNPs, haplotypes, and risk of NHL. Pre-chemotherapy organochlorine levels were measured and gene-environment interaction analysis was performed. Results The IVS1 + 4640G/A SNP was significantly associated with NHL risk, with an odds ratio of 1.32 (95% CI = 1.05-1.65) for G/A or A/A genotypes compared to the G/G genotype. Interactions were observed with PCB 118, a known inducer of AHR, and chlordane-related analytes oxychlordane and trans-nonachlor, although no interactions were statistically significant after controlling for multiple comparisons. The observed interactions were consistent across NHL subtypes. Conclusion Results suggest that the AHR gene may play a role in determining the risk of NHL with exposure to organochlorines, and highlight the importance of understanding gene-environment interactions.</abstract><cop>Dordrecht</cop><pub>Dordrecht : Springer Netherlands</pub><pmid>19821039</pmid><doi>10.1007/s10552-009-9429-5</doi><tpages>12</tpages></addata></record>
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source MEDLINE; SpringerLink Journals; Jstor Complete Legacy
subjects Adult
Aged
Alleles
Aryl hydrocarbon receptors
Basic Helix-Loop-Helix Transcription Factors
Biomedical and Life Sciences
Biomedicine
British Columbia
Cancer
Cancer Research
Case-Control Studies
Chemotherapy
Dioxins
Environmental Exposure
Environmental Pollutants - blood
Epidemiology
Exons
Genes
Genetic Predisposition to Disease
Genetic testing
Genotype
Genotypes
Haplotypes
Hematology
Humans
Hydrocarbons
Hydrocarbons, Chlorinated - blood
Kinases
Lymphoma
Lymphoma, Non-Hodgkin - epidemiology
Lymphoma, Non-Hodgkin - genetics
Middle Aged
Non Hodgkin lymphoma
Oncology
Original Paper
PCB
Pesticides
Plasma
Polychlorinated biphenyls
Polymorphism, Single Nucleotide
Public Health
Receptors, Aryl Hydrocarbon - genetics
Risk Factors
Sequencing
T lymphocytes
Toxicity
title Interaction between organochlorines and the AHR gene, and risk of non-Hodgkin lymphoma
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