Walter J Jessen1, Michael F Borgerding2, G L Prasad2. 1. a Laboratory Corporation of America Holdings (LabCorp) , Burlington , NC , USA. 2. b RAI Services Company , Winston-Salem , NC , USA.
Abstract
PURPOSE: Alternations in gene methylation and other epigenetic changes regulate normal development as well as drive disease progression. The aim of this study is to investigate global methylation changes in the buccal cells of smokers and smokeless tobacco users. MATERIALS AND METHODS: Generally healthy adult male subjects were recruited into smoker (SMK), moist snuff consumer (MSC) and non-tobacco consumer (NTC) cohorts (40 subjects/cohort) (ClinicalTrials.gov Identifier: NCT01923402). Global methylation profiling was performed on Illumina 450 K methylation arrays using buccal cell DNAs. RESULTS: The SMK cohort exhibited larger qualitative and quantitative changes relative to MSC. Approximately half of the differentially methylated 1252 gene loci were grouped as combustible tobacco-related (CTR) signatures and a third of the changes, tobacco-related (TR) signatures, were associated with smoking. Very few (41) differentially methylated gene loci were exclusively associated with moist snuff use and were designated as moist snuff-related (MSR) signature. Pathway enrichment analyses revealed that developmental and immune response pathways, among others, were impacted due to tobacco use. CONCLUSIONS: Chronic cigarette smoking causes hyper- and hypo-methylation of genes that could contribute to smoking-related diseases. These results help place combustible and non-combustible tobacco products along a risk continuum and provide additional insights into the effects of tobacco consumption.
PURPOSE: Alternations in gene methylation and other epigenetic changes regulate normal development as well as drive disease progression. The aim of this study is to investigate global methylation changes in the buccal cells of smokers and smokeless tobacco users. MATERIALS AND METHODS: Generally healthy adult male subjects were recruited into smoker (SMK), moist snuff consumer (MSC) and non-tobacco consumer (NTC) cohorts (40 subjects/cohort) (ClinicalTrials.gov Identifier: NCT01923402). Global methylation profiling was performed on Illumina 450 K methylation arrays using buccal cell DNAs. RESULTS: The SMK cohort exhibited larger qualitative and quantitative changes relative to MSC. Approximately half of the differentially methylated 1252 gene loci were grouped as combustible tobacco-related (CTR) signatures and a third of the changes, tobacco-related (TR) signatures, were associated with smoking. Very few (41) differentially methylated gene loci were exclusively associated with moist snuff use and were designated as moist snuff-related (MSR) signature. Pathway enrichment analyses revealed that developmental and immune response pathways, among others, were impacted due to tobacco use. CONCLUSIONS: Chronic cigarette smoking causes hyper- and hypo-methylation of genes that could contribute to smoking-related diseases. These results help place combustible and non-combustible tobacco products along a risk continuum and provide additional insights into the effects of tobacco consumption.
Authors: Andrei L Turinsky; Darci T Butcher; Sanaa Choufani; Rosanna Weksberg; Michael Brudno Journal: Epigenetics Date: 2019-03-01 Impact factor: 4.528
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