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Cigarette smoking and KRAS oncogene mutations in sporadic colorectal cancer: results from the Netherlands Cohort Study.
Mutat Res. 2008 Mar 29; 652(1):54-64.MR

Abstract

Since a KRAS oncogene mutation is an early event in colorectal cancer development and cigarette smoking is thought to have an effect on early stages of colorectal tumorigenesis, smoking, especially long-term smoking, may be associated with the risk for colorectal cancer with KRAS oncogene mutations. In the Netherlands Cohort Study on diet and cancer (n=120,852 men and women), using a case-cohort design, adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) were computed for colorectal tumors with wild-type and with mutated KRAS gene, and with specific G:C-->T:A or G:C-->A:T point mutations in KRAS, according to cigarette smoking status, frequency, duration, pack years, age at first exposure, years since cessation, inhalation and filter usage. After 7.3 years and excluding the first 2.3 years, 648 cases and 4083 sub-cohort members were included in the analyses. Ex-smokers, but not current smokers, were at increased risk for colorectal cancer with wild-type KRAS gene tumors when compared with never smokers, albeit not statistically significant (RR 1.26, 95% CI 0.96-1.66). This was not observed for KRAS mutated tumors when comparing ex-smokers with never smokers (RR 1.15, 95% CI 0.79-1.66). The highest category of smoking frequency (>20 cigarettes/day) and inhalation of smoke were associated with an increased risk for colorectal cancer with wild-type KRAS gene tumors, though not statistically significant, when compared with never smoking (frequency: RR 1.24, 95% CI 0.90-1.71 and inhalation: RR 1.25, 95% CI 0.94-1.67). These associations were strongest in men (ex-smokers: RR 1.79, 95% CI 1.00-3.20; frequency: RR 1.91, 95% CI 1.03-3.52; inhalation: RR 1.69, 95% CI 0.94-3.04). No associations were observed between any of the smoking characteristics and the risk for colorectal cancer with mutated KRAS gene tumors, nor where there any clear associations with tumors with specific G:C-->A:T transitions or G:C-->T:A transversions. These results suggest that, in contrast to the hypothesis, smoking does not increase the risk for colorectal tumors with a mutated KRAS gene. Some smoking characteristics, i.e. being an ex-smoker, frequency and inhalation, may be associated with risk for colorectal cancer characterized by the wild-type KRAS gene, especially in men.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Weijenberg MP
GROW-School for Oncology and Developmental Biology, University Maastricht, Department of Epidemiology, Maastricht University, Maastricht, The Netherlands. MP.Weijenberg@epid.unimaas.nl <MP.Weijenberg@epid.unimaas.nl>
Aardening PW
No affiliation info available
de Kok TM
No affiliation info available
de Goeij AF
No affiliation info available
van den Brandt PA
No affiliation info available

MeSH

AdenocarcinomaAgedAlcohol DrinkingCohort StudiesColorectal NeoplasmsFemaleFollow-Up StudiesGenes, rasGenetic LinkageHumansInhalation ExposureMaleMiddle AgedPoint MutationProspective StudiesRisk FactorsSex CharacteristicsSmokingSmoking CessationTime Factors

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18296105

Citation

Weijenberg, M P., et al. "Cigarette Smoking and KRAS Oncogene Mutations in Sporadic Colorectal Cancer: Results From the Netherlands Cohort Study." Mutation Research, vol. 652, no. 1, 2008, pp. 54-64.
Weijenberg MP, Aardening PW, de Kok TM, et al. Cigarette smoking and KRAS oncogene mutations in sporadic colorectal cancer: results from the Netherlands Cohort Study. Mutat Res. 2008;652(1):54-64.
Weijenberg, M. P., Aardening, P. W., de Kok, T. M., de Goeij, A. F., & van den Brandt, P. A. (2008). Cigarette smoking and KRAS oncogene mutations in sporadic colorectal cancer: results from the Netherlands Cohort Study. Mutation Research, 652(1), 54-64. https://doi.org/10.1016/j.mrgentox.2007.12.008
Weijenberg MP, et al. Cigarette Smoking and KRAS Oncogene Mutations in Sporadic Colorectal Cancer: Results From the Netherlands Cohort Study. Mutat Res. 2008 Mar 29;652(1):54-64. PubMed PMID: 18296105.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cigarette smoking and KRAS oncogene mutations in sporadic colorectal cancer: results from the Netherlands Cohort Study. AU - Weijenberg,M P, AU - Aardening,P W M, AU - de Kok,T M, AU - de Goeij,A F P M, AU - van den Brandt,P A, Y1 - 2008/01/11/ PY - 2007/03/06/received PY - 2007/11/16/revised PY - 2007/12/10/accepted PY - 2008/2/26/pubmed PY - 2008/5/29/medline PY - 2008/2/26/entrez SP - 54 EP - 64 JF - Mutation research JO - Mutat Res VL - 652 IS - 1 N2 - Since a KRAS oncogene mutation is an early event in colorectal cancer development and cigarette smoking is thought to have an effect on early stages of colorectal tumorigenesis, smoking, especially long-term smoking, may be associated with the risk for colorectal cancer with KRAS oncogene mutations. In the Netherlands Cohort Study on diet and cancer (n=120,852 men and women), using a case-cohort design, adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) were computed for colorectal tumors with wild-type and with mutated KRAS gene, and with specific G:C-->T:A or G:C-->A:T point mutations in KRAS, according to cigarette smoking status, frequency, duration, pack years, age at first exposure, years since cessation, inhalation and filter usage. After 7.3 years and excluding the first 2.3 years, 648 cases and 4083 sub-cohort members were included in the analyses. Ex-smokers, but not current smokers, were at increased risk for colorectal cancer with wild-type KRAS gene tumors when compared with never smokers, albeit not statistically significant (RR 1.26, 95% CI 0.96-1.66). This was not observed for KRAS mutated tumors when comparing ex-smokers with never smokers (RR 1.15, 95% CI 0.79-1.66). The highest category of smoking frequency (>20 cigarettes/day) and inhalation of smoke were associated with an increased risk for colorectal cancer with wild-type KRAS gene tumors, though not statistically significant, when compared with never smoking (frequency: RR 1.24, 95% CI 0.90-1.71 and inhalation: RR 1.25, 95% CI 0.94-1.67). These associations were strongest in men (ex-smokers: RR 1.79, 95% CI 1.00-3.20; frequency: RR 1.91, 95% CI 1.03-3.52; inhalation: RR 1.69, 95% CI 0.94-3.04). No associations were observed between any of the smoking characteristics and the risk for colorectal cancer with mutated KRAS gene tumors, nor where there any clear associations with tumors with specific G:C-->A:T transitions or G:C-->T:A transversions. These results suggest that, in contrast to the hypothesis, smoking does not increase the risk for colorectal tumors with a mutated KRAS gene. Some smoking characteristics, i.e. being an ex-smoker, frequency and inhalation, may be associated with risk for colorectal cancer characterized by the wild-type KRAS gene, especially in men. SN - 0027-5107 UR - https://www.unboundmedicine.com/medline/citation/18296105/Cigarette_smoking_and_KRAS_oncogene_mutations_in_sporadic_colorectal_cancer:_results_from_the_Netherlands_Cohort_Study_ DB - PRIME DP - Unbound Medicine ER -