Effects of smoking on genome-wide DNA methylation profiles: A study of discordant and concordant monozygotic twin pairs
Background: Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive mechanisms, but the contribution of a shared genetic predisposition to smoking and DNA methylation levels is typically not accounted for. Met...
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Published in | eLife Vol. 12 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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Cambridge
eLife Sciences Publications Ltd
10.08.2023
eLife Sciences Publications, Ltd |
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Abstract | Background:
Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive mechanisms, but the contribution of a shared genetic predisposition to smoking and DNA methylation levels is typically not accounted for.
Methods:
We exploited a strong within-family design, that is, the discordant monozygotic twin design, to study reactiveness of DNA methylation in blood cells to smoking and reversibility of methylation patterns upon quitting smoking. Illumina HumanMethylation450 BeadChip data were available for 769 monozygotic twin pairs (mean age = 36 years, range = 18–78, 70% female), including pairs discordant or concordant for current or former smoking.
Results:
In pairs discordant for current smoking, 13 differentially methylated CpGs were found between current smoking twins and their genetically identical co-twin who never smoked. Top sites include multiple CpGs in
CACNA1D
and
GNG12
, which encode subunits of a calcium voltage-gated channel and G protein, respectively. These proteins interact with the nicotinic acetylcholine receptor, suggesting that methylation levels at these CpGs might be reactive to nicotine exposure. All 13 CpGs have been previously associated with smoking in unrelated individuals and data from monozygotic pairs discordant for former smoking indicated that methylation patterns are to a large extent reversible upon smoking cessation. We further showed that differences in smoking level exposure for monozygotic twins who are both current smokers but differ in the number of cigarettes they smoke are reflected in their DNA methylation profiles.
Conclusions:
In conclusion, by analysing data from monozygotic twins, we robustly demonstrate that DNA methylation level in human blood cells is reactive to cigarette smoking.
Funding:
We acknowledge funding from the National Institute on Drug Abuse grant DA049867, the Netherlands Organization for Scientific Research (NWO): Biobanking and Biomolecular Research Infrastructure (BBMRI-NL, NWO 184.033.111) and the BBRMI-NL-financed BIOS Consortium (NWO 184.021.007), NWO Large Scale infrastructures X-Omics (184.034.019), Genotype/phenotype database for behaviour genetic and genetic epidemiological studies (ZonMw Middelgroot 911-09-032); Netherlands Twin Registry Repository: researching the interplay between genome and environment (NWO-Groot 480-15-001/674); the Avera Institute, Sioux Falls (USA), and the National Institutes of Health (NIH R01 HD042157-01A1, MH081802, Grand Opportunity grants 1RC2 MH089951 and 1RC2 MH089995); epigenetic data were generated at the Human Genomics Facility (HuGe-F) at ErasmusMC Rotterdam. Cotinine assaying was sponsored by the Neuroscience Campus Amsterdam. DIB acknowledges the Royal Netherlands Academy of Science Professor Award (PAH/6635).
The genetic information of people who smoke present distinctive characteristics. In particular, previous research has revealed differences in patterns of DNA methylation, a type of chemical modification that helps cells switch certain genes on or off. However, most of these studies could not establish for sure whether these changes were caused by smoking, predisposed individuals to smoke, or were driven by underlying genetic variation in the DNA sequence itself.
To investigate this question, van Dongen et al. examined DNA methylation data from the blood cells of over 700 pairs of identical twins. These individuals share the exact same genetic information, making it possible to better evaluate the impact of lifestyle on DNA modifications.
The analyses identified differences in methylation at 13 DNA locations in pairs of twins where one was a current smoker and their sibling had never smoked. Two of the genes code for proteins involved in the response to nicotine, the primary addictive chemical in cigarette smoke. The differences were smaller if one of the twins had stopped smoking, suggesting that quitting can help to reverse some of these changes.
These findings confirm that DNA methylation in blood cells is influenced by cigarette smoke, which could help to better understand smoking-associated diseases. They also demonstrate how useful identical twins studies can be to identify methylation changes that are markers of lifestyle. |
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AbstractList | Background: Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive mechanisms, but the contribution of a shared genetic predisposition to smoking and DNA methylation levels is typically not accounted for. Methods: We exploited a strong within-family design, that is, the discordant monozygotic twin design, to study reactiveness of DNA methylation in blood cells to smoking and reversibility of methylation patterns upon quitting smoking. Illumina HumanMethylation450 BeadChip data were available for 769 monozygotic twin pairs (mean age = 36 years, range = 18–78, 70% female), including pairs discordant or concordant for current or former smoking. Results: In pairs discordant for current smoking, 13 differentially methylated CpGs were found between current smoking twins and their genetically identical co-twin who never smoked. Top sites include multiple CpGs in CACNA1D and GNG12, which encode subunits of a calcium voltage-gated channel and G protein, respectively. These proteins interact with the nicotinic acetylcholine receptor, suggesting that methylation levels at these CpGs might be reactive to nicotine exposure. All 13 CpGs have been previously associated with smoking in unrelated individuals and data from monozygotic pairs discordant for former smoking indicated that methylation patterns are to a large extent reversible upon smoking cessation. We further showed that differences in smoking level exposure for monozygotic twins who are both current smokers but differ in the number of cigarettes they smoke are reflected in their DNA methylation profiles. Conclusions: In conclusion, by analysing data from monozygotic twins, we robustly demonstrate that DNA methylation level in human blood cells is reactive to cigarette smoking. Funding: We acknowledge funding from the National Institute on Drug Abuse grant DA049867, the Netherlands Organization for Scientific Research (NWO): Biobanking and Biomolecular Research Infrastructure (BBMRI-NL, NWO 184.033.111) and the BBRMI-NL-financed BIOS Consortium (NWO 184.021.007), NWO Large Scale infrastructures X-Omics (184.034.019), Genotype/phenotype database for behaviour genetic and genetic epidemiological studies (ZonMw Middelgroot 911-09-032); Netherlands Twin Registry Repository: researching the interplay between genome and environment (NWO-Groot 480-15-001/674); the Avera Institute, Sioux Falls (USA), and the National Institutes of Health (NIH R01 HD042157-01A1, MH081802, Grand Opportunity grants 1RC2 MH089951 and 1RC2 MH089995); epigenetic data were generated at the Human Genomics Facility (HuGe-F) at ErasmusMC Rotterdam. Cotinine assaying was sponsored by the Neuroscience Campus Amsterdam. DIB acknowledges the Royal Netherlands Academy of Science Professor Award (PAH/6635). The genetic information of people who smoke present distinctive characteristics. In particular, previous research has revealed differences in patterns of DNA methylation, a type of chemical modification that helps cells switch certain genes on or off. However, most of these studies could not establish for sure whether these changes were caused by smoking, predisposed individuals to smoke, or were driven by underlying genetic variation in the DNA sequence itself. To investigate this question, van Dongen et al. examined DNA methylation data from the blood cells of over 700 pairs of identical twins. These individuals share the exact same genetic information, making it possible to better evaluate the impact of lifestyle on DNA modifications. The analyses identified differences in methylation at 13 DNA locations in pairs of twins where one was a current smoker and their sibling had never smoked. Two of the genes code for proteins involved in the response to nicotine, the primary addictive chemical in cigarette smoke. The differences were smaller if one of the twins had stopped smoking, suggesting that quitting can help to reverse some of these changes. These findings confirm that DNA methylation in blood cells is influenced by cigarette smoke, which could help to better understand smoking-associated diseases. They also demonstrate how useful identical twins studies can be to identify methylation changes that are markers of lifestyle. Background: Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive mechanisms, but the contribution of a shared genetic predisposition to smoking and DNA methylation levels is typically not accounted for. Methods: We exploited a strong within-family design, that is, the discordant monozygotic twin design, to study reactiveness of DNA methylation in blood cells to smoking and reversibility of methylation patterns upon quitting smoking. Illumina HumanMethylation450 BeadChip data were available for 769 monozygotic twin pairs (mean age = 36 years, range = 18–78, 70% female), including pairs discordant or concordant for current or former smoking. Results: In pairs discordant for current smoking, 13 differentially methylated CpGs were found between current smoking twins and their genetically identical co-twin who never smoked. Top sites include multiple CpGs in CACNA1D and GNG12 , which encode subunits of a calcium voltage-gated channel and G protein, respectively. These proteins interact with the nicotinic acetylcholine receptor, suggesting that methylation levels at these CpGs might be reactive to nicotine exposure. All 13 CpGs have been previously associated with smoking in unrelated individuals and data from monozygotic pairs discordant for former smoking indicated that methylation patterns are to a large extent reversible upon smoking cessation. We further showed that differences in smoking level exposure for monozygotic twins who are both current smokers but differ in the number of cigarettes they smoke are reflected in their DNA methylation profiles. Conclusions: In conclusion, by analysing data from monozygotic twins, we robustly demonstrate that DNA methylation level in human blood cells is reactive to cigarette smoking. Funding: We acknowledge funding from the National Institute on Drug Abuse grant DA049867, the Netherlands Organization for Scientific Research (NWO): Biobanking and Biomolecular Research Infrastructure (BBMRI-NL, NWO 184.033.111) and the BBRMI-NL-financed BIOS Consortium (NWO 184.021.007), NWO Large Scale infrastructures X-Omics (184.034.019), Genotype/phenotype database for behaviour genetic and genetic epidemiological studies (ZonMw Middelgroot 911-09-032); Netherlands Twin Registry Repository: researching the interplay between genome and environment (NWO-Groot 480-15-001/674); the Avera Institute, Sioux Falls (USA), and the National Institutes of Health (NIH R01 HD042157-01A1, MH081802, Grand Opportunity grants 1RC2 MH089951 and 1RC2 MH089995); epigenetic data were generated at the Human Genomics Facility (HuGe-F) at ErasmusMC Rotterdam. Cotinine assaying was sponsored by the Neuroscience Campus Amsterdam. DIB acknowledges the Royal Netherlands Academy of Science Professor Award (PAH/6635). The genetic information of people who smoke present distinctive characteristics. In particular, previous research has revealed differences in patterns of DNA methylation, a type of chemical modification that helps cells switch certain genes on or off. However, most of these studies could not establish for sure whether these changes were caused by smoking, predisposed individuals to smoke, or were driven by underlying genetic variation in the DNA sequence itself. To investigate this question, van Dongen et al. examined DNA methylation data from the blood cells of over 700 pairs of identical twins. These individuals share the exact same genetic information, making it possible to better evaluate the impact of lifestyle on DNA modifications. The analyses identified differences in methylation at 13 DNA locations in pairs of twins where one was a current smoker and their sibling had never smoked. Two of the genes code for proteins involved in the response to nicotine, the primary addictive chemical in cigarette smoke. The differences were smaller if one of the twins had stopped smoking, suggesting that quitting can help to reverse some of these changes. These findings confirm that DNA methylation in blood cells is influenced by cigarette smoke, which could help to better understand smoking-associated diseases. They also demonstrate how useful identical twins studies can be to identify methylation changes that are markers of lifestyle. Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive mechanisms, but the contribution of a shared genetic predisposition to smoking and DNA methylation levels is typically not accounted for.BackgroundSmoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive mechanisms, but the contribution of a shared genetic predisposition to smoking and DNA methylation levels is typically not accounted for.We exploited a strong within-family design, that is, the discordant monozygotic twin design, to study reactiveness of DNA methylation in blood cells to smoking and reversibility of methylation patterns upon quitting smoking. Illumina HumanMethylation450 BeadChip data were available for 769 monozygotic twin pairs (mean age = 36 years, range = 18-78, 70% female), including pairs discordant or concordant for current or former smoking.MethodsWe exploited a strong within-family design, that is, the discordant monozygotic twin design, to study reactiveness of DNA methylation in blood cells to smoking and reversibility of methylation patterns upon quitting smoking. Illumina HumanMethylation450 BeadChip data were available for 769 monozygotic twin pairs (mean age = 36 years, range = 18-78, 70% female), including pairs discordant or concordant for current or former smoking.In pairs discordant for current smoking, 13 differentially methylated CpGs were found between current smoking twins and their genetically identical co-twin who never smoked. Top sites include multiple CpGs in CACNA1D and GNG12, which encode subunits of a calcium voltage-gated channel and G protein, respectively. These proteins interact with the nicotinic acetylcholine receptor, suggesting that methylation levels at these CpGs might be reactive to nicotine exposure. All 13 CpGs have been previously associated with smoking in unrelated individuals and data from monozygotic pairs discordant for former smoking indicated that methylation patterns are to a large extent reversible upon smoking cessation. We further showed that differences in smoking level exposure for monozygotic twins who are both current smokers but differ in the number of cigarettes they smoke are reflected in their DNA methylation profiles.ResultsIn pairs discordant for current smoking, 13 differentially methylated CpGs were found between current smoking twins and their genetically identical co-twin who never smoked. Top sites include multiple CpGs in CACNA1D and GNG12, which encode subunits of a calcium voltage-gated channel and G protein, respectively. These proteins interact with the nicotinic acetylcholine receptor, suggesting that methylation levels at these CpGs might be reactive to nicotine exposure. All 13 CpGs have been previously associated with smoking in unrelated individuals and data from monozygotic pairs discordant for former smoking indicated that methylation patterns are to a large extent reversible upon smoking cessation. We further showed that differences in smoking level exposure for monozygotic twins who are both current smokers but differ in the number of cigarettes they smoke are reflected in their DNA methylation profiles.In conclusion, by analysing data from monozygotic twins, we robustly demonstrate that DNA methylation level in human blood cells is reactive to cigarette smoking.ConclusionsIn conclusion, by analysing data from monozygotic twins, we robustly demonstrate that DNA methylation level in human blood cells is reactive to cigarette smoking.We acknowledge funding from the National Institute on Drug Abuse grant DA049867, the Netherlands Organization for Scientific Research (NWO): Biobanking and Biomolecular Research Infrastructure (BBMRI-NL, NWO 184.033.111) and the BBRMI-NL-financed BIOS Consortium (NWO 184.021.007), NWO Large Scale infrastructures X-Omics (184.034.019), Genotype/phenotype database for behaviour genetic and genetic epidemiological studies (ZonMw Middelgroot 911-09-032); Netherlands Twin Registry Repository: researching the interplay between genome and environment (NWO-Groot 480-15-001/674); the Avera Institute, Sioux Falls (USA), and the National Institutes of Health (NIH R01 HD042157-01A1, MH081802, Grand Opportunity grants 1RC2 MH089951 and 1RC2 MH089995); epigenetic data were generated at the Human Genomics Facility (HuGe-F) at ErasmusMC Rotterdam. Cotinine assaying was sponsored by the Neuroscience Campus Amsterdam. DIB acknowledges the Royal Netherlands Academy of Science Professor Award (PAH/6635).FundingWe acknowledge funding from the National Institute on Drug Abuse grant DA049867, the Netherlands Organization for Scientific Research (NWO): Biobanking and Biomolecular Research Infrastructure (BBMRI-NL, NWO 184.033.111) and the BBRMI-NL-financed BIOS Consortium (NWO 184.021.007), NWO Large Scale infrastructures X-Omics (184.034.019), Genotype/phenotype database for behaviour genetic and genetic epidemiological studies (ZonMw Middelgroot 911-09-032); Netherlands Twin Registry Repository: researching the interplay between genome and environment (NWO-Groot 480-15-001/674); the Avera Institute, Sioux Falls (USA), and the National Institutes of Health (NIH R01 HD042157-01A1, MH081802, Grand Opportunity grants 1RC2 MH089951 and 1RC2 MH089995); epigenetic data were generated at the Human Genomics Facility (HuGe-F) at ErasmusMC Rotterdam. Cotinine assaying was sponsored by the Neuroscience Campus Amsterdam. DIB acknowledges the Royal Netherlands Academy of Science Professor Award (PAH/6635). |
Author | van Dongen, Jenny Willemsen, Gonneke Boomsma, Dorret I de Geus, Eco JC Neale, Michael C |
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References | Liu (bib21) 2018; 23 Heikkinen (bib13) 2022; 292 Rodgman (bib30) 2008 The Genome of the Netherlands Consortium (bib38) 2014; 46 Joehanes (bib14) 2016; 9 van Dongen (bib41) 2018; 3 Willemsen (bib46) 2010; 13 Smith (bib35) 2000; 38 Minică (bib24) 2018; 48 Bot (bib5) 2013; 75 the BIOS Consortium (bib37) 2017; 49 Ligthart (bib20) 2019; 22 van Dongen (bib40) 2016; 7 Benhammou (bib3) 2000; 39 Lee (bib16) 2013; 4 Allione (bib1) 2015; 10 Zillich (bib47) 2022; 12 Satta (bib31) 2008; 105 Martin (bib23) 1997; 17 van Iterson (bib43) 2017; 18 Sinke (bib34) 2020 Sinke (bib33) 2019 Vink (bib45) 2017; 22 Hancock (bib12) 2018; 23 Cuozzo (bib7) 2007; 3 Jonsson (bib15) 2021; 53 Shen (bib32) 2009; 30 Gao (bib9) 2015; 7 Gupta (bib10) 2019; 11 Tsai (bib39) 2015; 44 Leeuwen (bib18) 2007; 28 van Rooij (bib44) 2019; 20 Lee (bib17) 2016; 8 Fortin (bib8) 2014; 15 Li (bib19) 2019; 47 Hall (bib11) 1996; 6 van Iterson (bib42) 2014; 30 Bell (bib2) 2012; 13 Peng (bib28) 2022; 12 Liu (bib22) 2019; 51 Talhout (bib36) 2011; 8 Bibikova (bib4) 2011; 98 Olson (bib26) 1984; 1 Ouwens (bib27) 2018; 39 Chen (bib6) 2013; 8 R Development Core Team (bib29) 2013 Mortusewicz (bib25) 2005; 102 |
References_xml | – volume: 9 start-page: 436 year: 2016 ident: bib14 article-title: Epigenetic signatures of cigarette smoking publication-title: Circulation. Cardiovascular Genetics doi: 10.1161/CIRCGENETICS.116.001506 contributor: fullname: Joehanes – volume: 13 start-page: 1 year: 2012 ident: bib2 article-title: DNA methylation studies using twins: what are they telling us? publication-title: Genome Biology doi: 10.1186/gb-2012-13-10-172 contributor: fullname: Bell – volume: 6 start-page: 343 year: 1996 ident: bib11 article-title: Twinning: mechanisms and genetic implications publication-title: Current Opinion in Genetics & Development doi: 10.1016/s0959-437x(96)80012-8 contributor: fullname: Hall – volume: 51 start-page: 237 year: 2019 ident: bib22 article-title: Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use publication-title: Nature Genetics doi: 10.1038/s41588-018-0307-5 contributor: fullname: Liu – volume-title: The chemical components of tobacco and tobacco smoke year: 2008 ident: bib30 doi: 10.1201/9781420078848 contributor: fullname: Rodgman – volume: 30 start-page: 673 year: 2009 ident: bib32 article-title: Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system publication-title: Acta Pharmacologica Sinica doi: 10.1038/aps.2009.64 contributor: fullname: Shen – volume: 17 start-page: 387 year: 1997 ident: bib23 article-title: A twin-pronged attack on complex traits publication-title: Nature Genetics doi: 10.1038/ng1297-387 contributor: fullname: Martin – volume-title: Software Heritage year: 2020 ident: bib34 article-title: Dnamarray_Workflow contributor: fullname: Sinke – volume: 11 year: 2019 ident: bib10 article-title: Epigenome-wide association study of serum cotinine in current smokers reveals novel genetically driven loci publication-title: Clinical Epigenetics doi: 10.1186/s13148-018-0606-9 contributor: fullname: Gupta – volume: 292 start-page: 390 year: 2022 ident: bib13 article-title: The potential of DNA methylation as a biomarker for obesity and smoking publication-title: Journal of Internal Medicine doi: 10.1111/joim.13496 contributor: fullname: Heikkinen – volume: 46 start-page: 818 year: 2014 ident: bib38 article-title: Whole-genome sequence variation, population structure and demographic history of the Dutch population publication-title: Nature Genetics doi: 10.1038/ng.3021 contributor: fullname: The Genome of the Netherlands Consortium – volume: 75 start-page: 431 year: 2013 ident: bib5 article-title: Exposure to secondhand smoke and depression and anxiety: a report from two studies in the Netherlands publication-title: Journal of Psychosomatic Research doi: 10.1016/j.jpsychores.2013.08.016 contributor: fullname: Bot – volume: 12 year: 2022 ident: bib47 article-title: Epigenetic signatures of smoking in five brain regions publication-title: Journal of Personalized Medicine doi: 10.3390/jpm12040566 contributor: fullname: Zillich – volume: 53 start-page: 27 year: 2021 ident: bib15 article-title: Differences between germline genomes of monozygotic twins publication-title: Nature Genetics doi: 10.1038/s41588-020-00755-1 contributor: fullname: Jonsson – volume: 102 start-page: 8905 year: 2005 ident: bib25 article-title: Recruitment of DNA methyltransferase I to DNA repair sites publication-title: PNAS doi: 10.1073/pnas.0501034102 contributor: fullname: Mortusewicz – volume: 23 start-page: 422 year: 2018 ident: bib21 article-title: A DNA methylation biomarker of alcohol consumption publication-title: Molecular Psychiatry doi: 10.1038/mp.2016.192 contributor: fullname: Liu – volume: 105 start-page: 16356 year: 2008 ident: bib31 article-title: Nicotine decreases DNA methyltransferase 1 expression and glutamic acid decarboxylase 67 promoter methylation in GABAergic interneurons publication-title: PNAS doi: 10.1073/pnas.0808699105 contributor: fullname: Satta – volume: 38 start-page: 637 year: 2000 ident: bib35 article-title: The relative toxicity of compounds in mainstream cigarette smoke condensate publication-title: Food and Chemical Toxicology doi: 10.1016/s0278-6915(00)00051-x contributor: fullname: Smith – volume: 3 year: 2018 ident: bib41 article-title: DNA methylation signatures of educational attainment publication-title: NPJ Science of Learning doi: 10.1038/s41539-018-0020-2 contributor: fullname: van Dongen – volume: 30 start-page: 3435 year: 2014 ident: bib42 article-title: MethylAid: visual and interactive quality control of large Illumina 450k datasets publication-title: Bioinformatics doi: 10.1093/bioinformatics/btu566 contributor: fullname: van Iterson – volume: 39 start-page: 2818 year: 2000 ident: bib3 article-title: [(3)H]Nicotine binding in peripheral blood cells of smokers is correlated with the number of cigarettes smoked per day publication-title: Neuropharmacology doi: 10.1016/s0028-3908(00)00153-2 contributor: fullname: Benhammou – volume: 7 year: 2016 ident: bib40 article-title: Genetic and environmental influences interact with age and sex in shaping the human methylome publication-title: Nature Communications doi: 10.1038/ncomms11115 contributor: fullname: van Dongen – volume: 20 year: 2019 ident: bib44 article-title: Evaluation of commonly used analysis strategies for epigenome- and transcriptome-wide association studies through replication of large-scale population studies publication-title: Genome Biology doi: 10.1186/s13059-019-1878-x contributor: fullname: van Rooij – volume: 47 start-page: D983 year: 2019 ident: bib19 article-title: EWAS Atlas: A curated knowledgebase of epigenome-wide association studies publication-title: Nucleic Acids Research doi: 10.1093/nar/gky1027 contributor: fullname: Li – volume: 28 start-page: 691 year: 2007 ident: bib18 article-title: Cigarette smoke-induced differential gene expression in blood cells from monozygotic twin pairs publication-title: Carcinogenesis doi: 10.1093/carcin/bgl199 contributor: fullname: Leeuwen – volume: 3 year: 2007 ident: bib7 article-title: DNA damage, homology-directed repair, and DNA methylation publication-title: PLOS Genetics doi: 10.1371/journal.pgen.0030110 contributor: fullname: Cuozzo – volume: 98 start-page: 288 year: 2011 ident: bib4 article-title: High density DNA methylation array with single CpG site resolution publication-title: Genomics doi: 10.1016/j.ygeno.2011.07.007 contributor: fullname: Bibikova – volume: 8 start-page: 203 year: 2013 ident: bib6 article-title: Discovery of cross-reactive probes and polymorphic CpGs in the Illumina Infinium HumanMethylation450 microarray publication-title: Epigenetics doi: 10.4161/epi.23470 contributor: fullname: Chen – volume: 49 start-page: 131 year: 2017 ident: bib37 article-title: Disease variants alter transcription factor levels and methylation of their binding sites publication-title: Nature Genetics doi: 10.1038/ng.3721 contributor: fullname: the BIOS Consortium – year: 2013 ident: bib29 article-title: R: A language and environment for statistical computing contributor: fullname: R Development Core Team – volume: 8 start-page: 613 year: 2011 ident: bib36 article-title: Hazardous compounds in tobacco smoke publication-title: International Journal of Environmental Research and Public Health doi: 10.3390/ijerph8020613 contributor: fullname: Talhout – volume: 18 year: 2017 ident: bib43 article-title: Controlling bias and inflation in epigenome- and transcriptome-wide association studies using the empirical null distribution publication-title: Genome Biology doi: 10.1186/s13059-016-1131-9 contributor: fullname: van Iterson – volume: 22 start-page: 623 year: 2019 ident: bib20 article-title: The netherlands twin register: longitudinal research based on twin and twin-family designs publication-title: Twin Research and Human Genetics doi: 10.1017/thg.2019.93 contributor: fullname: Ligthart – volume: 22 start-page: 550 year: 2017 ident: bib45 article-title: Differential gene expression patterns between smokers and non-smokers: cause or consequence? publication-title: Addiction Biology doi: 10.1111/adb.12322 contributor: fullname: Vink – volume: 1 start-page: 233 year: 1984 ident: bib26 article-title: Carbon monoxide poisoning: mechanisms, presentation, and controversies in management publication-title: The Journal of Emergency Medicine doi: 10.1016/0736-4679(84)90078-7 contributor: fullname: Olson – volume: 10 year: 2015 ident: bib1 article-title: Novel epigenetic changes unveiled by monozygotic twins discordant for smoking habits publication-title: PLOS ONE doi: 10.1371/journal.pone.0128265 contributor: fullname: Allione – volume-title: Zenodo year: 2019 ident: bib33 article-title: Streamlined Workflow for the quality control, normalization, and analysis of Illumina methylation array data - the Leiden approach doi: 10.5281/zenodo.3355292 contributor: fullname: Sinke – volume: 39 start-page: 1393 year: 2018 ident: bib27 article-title: A characterization of postzygotic mutations identified in monozygotic twins publication-title: Human Mutation doi: 10.1002/humu.23586 contributor: fullname: Ouwens – volume: 48 start-page: 337 year: 2018 ident: bib24 article-title: Extending causality tests with genetic instruments: an integration of mendelian randomization with the classical twin design publication-title: Behavior Genetics doi: 10.1007/s10519-018-9904-4 contributor: fullname: Minică – volume: 7 year: 2015 ident: bib9 article-title: DNA methylation changes of whole blood cells in response to active smoking exposure in adults: a systematic review of DNA methylation studies publication-title: Clinical Epigenetics doi: 10.1186/s13148-015-0148-3 contributor: fullname: Gao – volume: 15 year: 2014 ident: bib8 article-title: Functional normalization of 450k methylation array data improves replication in large cancer studies publication-title: Genome Biology doi: 10.1186/s13059-014-0503-2 contributor: fullname: Fortin – volume: 8 year: 2016 ident: bib17 article-title: DNA methylation and smoking in Korean adults: epigenome-wide association study publication-title: Clinical Epigenetics doi: 10.1186/s13148-016-0266-6 contributor: fullname: Lee – volume: 44 start-page: 1429 year: 2015 ident: bib39 article-title: Power and sample size estimation for epigenome-wide association scans to detect differential DNA methylation publication-title: International Journal of Epidemiology doi: 10.1093/ije/dyv041 contributor: fullname: Tsai – volume: 23 start-page: 1911 year: 2018 ident: bib12 article-title: Genome-wide association study across European and African American ancestries identifies a SNP in DNMT3B contributing to nicotine dependence publication-title: Molecular Psychiatry doi: 10.1038/mp.2017.193 contributor: fullname: Hancock – volume: 4 year: 2013 ident: bib16 article-title: Cigarette smoking and DNA methylation publication-title: Frontiers in Genetics doi: 10.3389/fgene.2013.00132 contributor: fullname: Lee – volume: 13 start-page: 231 year: 2010 ident: bib46 article-title: The Netherlands Twin Register biobank: a resource for genetic epidemiological studies publication-title: Twin Research and Human Genetics doi: 10.1375/twin.13.3.231 contributor: fullname: Willemsen – volume: 12 start-page: 3679 year: 2022 ident: bib28 article-title: Nicotine dose-dependent epigenomic-wide DNA methylation changes in the mice with long-term electronic cigarette exposure publication-title: American Journal of Cancer Research contributor: fullname: Peng |
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Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive... Background:Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive... Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive mechanisms,... The genetic information of people who smoke present distinctive characteristics. In particular, previous research has revealed differences in patterns of DNA... Background: Smoking-associated DNA methylation levels identified through epigenome-wide association studies (EWASs) are generally ascribed to smoking-reactive... |
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SubjectTerms | Acetylcholine receptors (nicotinic) Biobanks Blood cells Calcium channels (voltage-gated) Channel gating Cigarette smoking Consortia Cotinine discordant twins Disease DNA methylation Drug abuse Drug addiction Epidemiology Epidemiology and Global Health Epigenetics Genetics and Genomics Genomes Genotypes Health behavior identical twins Native North Americans Phenotypes Quality control Smoking cessation Twin studies twin study Twins |
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Title | Effects of smoking on genome-wide DNA methylation profiles: A study of discordant and concordant monozygotic twin pairs |
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