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Are SNP-Smoking Association Studies Needed in Controls? DNA Repair Gene Polymorphisms and Smoking Intensity.

Verde Z, Reinoso L, Chicharro LM, Resano P, Sánchez-Hernández I, Rodríguez González-Moro JM, Bandrés F, Gómez-Gallego F, Santiago C - PLoS ONE (2015)

Bottom Line: Common problems in genetic association studies, such as presence of gene-by-environment (G x E) correlation in the population, may reduce the validity of these designs.We found an association between the wild type alleles of XRCC3 Thr241Met or KLC3 Lys751Gln and greater smoking intensity (OR = 12.98, 95% CI = 2.86-58.82 and OR=16.90, 95% CI=2.09-142.8; respectively).Population-specific G x E studies should be carried out when genetic and environmental factors interact to cause the disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Morphological Sciences and Biomedicine, Universidad Europea, Madrid, Spain.

ABSTRACT
Variations in tobacco-related cancers, incidence and prevalence reflect differences in tobacco consumption in addition to genetic factors. Besides, genes related to lung cancer risk could be related to smoking behavior. Polymorphisms altering DNA repair capacity may lead to synergistic effects with tobacco carcinogen-induced lung cancer risk. Common problems in genetic association studies, such as presence of gene-by-environment (G x E) correlation in the population, may reduce the validity of these designs. The main purpose of this study was to evaluate the independence assumption for selected SNPs and smoking behaviour in a cohort of 320 healthy Spanish smokers. We found an association between the wild type alleles of XRCC3 Thr241Met or KLC3 Lys751Gln and greater smoking intensity (OR = 12.98, 95% CI = 2.86-58.82 and OR=16.90, 95% CI=2.09-142.8; respectively). Although preliminary, the results of our study provide evidence that genetic variations in DNA-repair genes may influence both smoking habits and the development of lung cancer. Population-specific G x E studies should be carried out when genetic and environmental factors interact to cause the disease.

No MeSH data available.


Related in: MedlinePlus

Association of CO levels and cigarettes reported.Note: The smokers were divided considering CO levels (ppm) into: very light smoker (0–6), light smoker (7–10), smoker (11–20) and heavy smoker (>20). Abbreviations: CPD, cigarettes per day.
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pone.0129374.g001: Association of CO levels and cigarettes reported.Note: The smokers were divided considering CO levels (ppm) into: very light smoker (0–6), light smoker (7–10), smoker (11–20) and heavy smoker (>20). Abbreviations: CPD, cigarettes per day.

Mentions: In order to check the number of CPD reported, the levels of CO (ppm) expired were tested in each smoker, resulting the following percentage in each category: very light smoker (19.6%), light smoker (15.6%), smoker (39.2%), and heavy smoker (25.6%). Statistically significant differences were found (P<0.001) among the following categories: very light smoker 9.77 CPD (SD = 6.52), light smoker 12.86 CPD (SD = 7.11), smoker 19.58 CPD (SD = 10.43), and heavy smoker 22.94 CPD (SD = 10.69). In addition, significant differences were found between PYS and CO levels (P<0.001): very light smoker 11.52 PYS (SD = 10.88), light smoker 14.91 PYS (SD = 10.38), smoker 24.38 PYS (SD = 22.06), and heavy smoker 29.43 PYS (SD = 19.68) (Figs 1 and 2).


Are SNP-Smoking Association Studies Needed in Controls? DNA Repair Gene Polymorphisms and Smoking Intensity.

Verde Z, Reinoso L, Chicharro LM, Resano P, Sánchez-Hernández I, Rodríguez González-Moro JM, Bandrés F, Gómez-Gallego F, Santiago C - PLoS ONE (2015)

Association of CO levels and cigarettes reported.Note: The smokers were divided considering CO levels (ppm) into: very light smoker (0–6), light smoker (7–10), smoker (11–20) and heavy smoker (>20). Abbreviations: CPD, cigarettes per day.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4446361&req=5

pone.0129374.g001: Association of CO levels and cigarettes reported.Note: The smokers were divided considering CO levels (ppm) into: very light smoker (0–6), light smoker (7–10), smoker (11–20) and heavy smoker (>20). Abbreviations: CPD, cigarettes per day.
Mentions: In order to check the number of CPD reported, the levels of CO (ppm) expired were tested in each smoker, resulting the following percentage in each category: very light smoker (19.6%), light smoker (15.6%), smoker (39.2%), and heavy smoker (25.6%). Statistically significant differences were found (P<0.001) among the following categories: very light smoker 9.77 CPD (SD = 6.52), light smoker 12.86 CPD (SD = 7.11), smoker 19.58 CPD (SD = 10.43), and heavy smoker 22.94 CPD (SD = 10.69). In addition, significant differences were found between PYS and CO levels (P<0.001): very light smoker 11.52 PYS (SD = 10.88), light smoker 14.91 PYS (SD = 10.38), smoker 24.38 PYS (SD = 22.06), and heavy smoker 29.43 PYS (SD = 19.68) (Figs 1 and 2).

Bottom Line: Common problems in genetic association studies, such as presence of gene-by-environment (G x E) correlation in the population, may reduce the validity of these designs.We found an association between the wild type alleles of XRCC3 Thr241Met or KLC3 Lys751Gln and greater smoking intensity (OR = 12.98, 95% CI = 2.86-58.82 and OR=16.90, 95% CI=2.09-142.8; respectively).Population-specific G x E studies should be carried out when genetic and environmental factors interact to cause the disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Morphological Sciences and Biomedicine, Universidad Europea, Madrid, Spain.

ABSTRACT
Variations in tobacco-related cancers, incidence and prevalence reflect differences in tobacco consumption in addition to genetic factors. Besides, genes related to lung cancer risk could be related to smoking behavior. Polymorphisms altering DNA repair capacity may lead to synergistic effects with tobacco carcinogen-induced lung cancer risk. Common problems in genetic association studies, such as presence of gene-by-environment (G x E) correlation in the population, may reduce the validity of these designs. The main purpose of this study was to evaluate the independence assumption for selected SNPs and smoking behaviour in a cohort of 320 healthy Spanish smokers. We found an association between the wild type alleles of XRCC3 Thr241Met or KLC3 Lys751Gln and greater smoking intensity (OR = 12.98, 95% CI = 2.86-58.82 and OR=16.90, 95% CI=2.09-142.8; respectively). Although preliminary, the results of our study provide evidence that genetic variations in DNA-repair genes may influence both smoking habits and the development of lung cancer. Population-specific G x E studies should be carried out when genetic and environmental factors interact to cause the disease.

No MeSH data available.


Related in: MedlinePlus