Cigarette Smoking and Colorectal Cancer: APC Mutations, hMLH1 Expression, and GSTM1 and GSTT1 Polymorphisms

Lüchtenborg, Margreet; Weijenberg, Matty P.; Kampman, Ellen; Muijen, G N van; Roemen, Guido M.J.M.; Zeegers, Maurice P.; Goldbohm, R. Alexandra; Veer, P. van ‘t; Goeij, Anton F.P.M. de; Brandt, Piet A. van den

doi:10.1093/aje/kwi114

Cited by 54 publications

(41 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…99,100 Our finding of no interaction between GSTM1 genotype and smoking is consistent with the pooled analysis of Smits et al 64 and with other studies. [101][102][103][104][105] As in the present study, other studies do not suggest an interaction between GSTM1 genotype and meat intake. 98,103,106,107 Similar to the findings of Turner et al, 96 our data did not suggest an interaction between GSTM1 genotype and intake of green leafy vegetables.…”

Section: Discussionsupporting

confidence: 58%

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

Little

Sharp

Masson

et al. 2006

Intl Journal of Cancer

View full text Add to dashboard Cite

Cytochrome P-450 CYP1A1 is involved in the metabolism of polycyclic aromatic hydrocarbons (PAHs) that are derived from meat intake and tobacco smoking. Expression of the CYP1A1 gene is induced by compounds present in cruciferous vegetables. The glutathione S-transferases play a central role in the detoxification of carcinogens, including PAHs. We investigated the association between colorectal cancer and three variants (CYP1A1*2A, CYP1A1*2C, CYP1A1*4) of the CYP1A1 gene, and homozygosity for the null deletion of the GSTM1 and GSTT1 genes, and the joint effects of these genotypes and smoking, meat intake and intake of green leafy vegetables in a population-based study of 264 cases and 408 controls in Northeast Scotland. There was an inverse association with the CYP1A1*4 (m4) variant (OR 0.3, 95% CI 0.13-0.70). The OR for the CYP1A1*2C (m2) variant was 1.3 (95% CI 0.59-2.91), which is similar to a combined estimate for previous studies (OR 1.2, 95% CI 0.95-1.41). We observed no association with the CYP1A1*2A (m1) variant, or the GSTM1 and GSTT1 polymorphisms. Significant interactions between all 3 CYP1A1 variants and meat intake, and between the m1 and m2 variants and intake of green leafy vegetables, were observed. There was no evidence of interaction between CYP1A1 and smoking, and no evidence of interaction between the GSTM1 or GSTT1 polymorphisms and smoking, meat intake, green leafy vegetable intake, CYP1A1 variants or each other. ' 2006 Wiley-Liss, Inc.Key words: colorectal neoplasms; cytochrome P-450 CYP1A1; GSTM1 protein; glutathione S-transferase T1; polymorphism Evidence on the association between colorectal cancer and consumption of cooked meats, 1 tobacco smoking 2,3 and vegetable intake, 4-6 all of which are modifiable exposures with a potentially major public health impact, is inconsistent. Randomized trials 7,8 have confirmed evidence from most observational studies, [9][10][11][12] indicating an inverse relation between postmenopausal oestrogen replacement therapy and colorectal cancer, but considerable heterogeneity in the magnitude of this association was apparent. It is possible that these inconsistencies are in part due to differences between populations in the frequency of variants of genes, whose products modulate the effects of these exposures.A possible unifying factor underlying exposure to cooked meats, tobacco smoke and postmenopausal oestrogen replacement therapy is the presence of polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines. Cooking of meat and fish results in the formation of PAHs and, particularly at high temperatures, heterocyclic amines, which are carcinogenic in animals. [13][14][15] Tobacco smoking is another source of PAH exposure.16 PAHs affect oestrogen production and metabolism. 17CYP1A1 is expressed in the large bowel. 18,19 Because of the involvement of CYP1A1 in the metabolism of PAHs and oestrogens, and perhaps cruciferous vegetables and heterocyclic amines [20][21][22][23][24][25] (Table I), it might be expected that CYP1A1 variants might influence t...

show abstract

Section: Discussionsupporting

confidence: 58%

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

Little

Sharp

Masson

et al. 2006

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Some (34,(49)(50)(51) but not all(52-54) prior studies have reported a lack of association between smoking and colorectal cancer. Other studies have examined cofactors such as subject's metabolic genotype in tobacco carcinogen metabolism (55,56) and tumour characteristics (55,57) and found smoking to be associated with subgroups defined by these cofactors.…”

Section: Discussionmentioning

confidence: 99%

Morbidity and mortality in relation to smoking among women and men of Chinese ethnicity: The Singapore Chinese Health Study

Shankar¹,

Yuan²,

Koh³

et al. 2008

European Journal of Cancer

View full text Add to dashboard Cite

Objectives-We examined the association among cigarette smoking, smoking cessation and a broad range of cancer incidence and all cause and cause-specific mortality in a population-based cohort of adults of Chinese ethnicity in Singapore.Methods-Subjects were 61,320 participants of the Singapore Chinese Health Study (44.5% men, aged 45-74 years, recruitment from 1993-1998) who were free of cancer at the baseline examination. Main outcomes-of-interest included cancer incidence, all cause and cause-specific mortality as of December 31, 2005.Results-Cigarette smoking was positively associated with overall cancer incidence, including cancers at the following specific sites: head and neck region, upper gastrointestinal tract, hepatobiliary and pancreas cancer, lung, and bladder/renal pelvis cancer. Compared to never smokers, the relative risk (RR) (95% confidence interval [CI]) of cancer incidence (all cancer sites) among current smokers smoking >22 cigarettes/day was 1.9 (1.7-2.1), p-trend<0.0001. Similarly, cigarette smoking was associated with all cause and cause-specific mortality, including deaths due to cancer, ischemic heart disease, other heart diseases, and chronic obstructive pulmonary disease. Compared to never smokers, RR (95%CI) of all cause mortality among current smokers smoking >22 cigarettes/day was 1.8 (1.6-2.0), p-trend<0.0001. Also, relative to current smokers, ex-smokers experienced reduced cancer incidence and total mortality. The population attributable risk of smoking in men for cancer incidence as well as all-cause mortality was 23%, whereas in women it ranged from 4-5%.Conclusions-Cigarette smoking is an important risk factor for cancer incidence and major causes of mortality in Chinese men and women of Singapore.

show abstract

“…In the questionnaire, tobacco smoking was addressed through questions on smoking status (never, former, or current smoker) and inhalation for cigarette, cigar, and pipe smokers (26,27).…”

Section: Exposure Assessmentmentioning

confidence: 99%

Active and Passive Smoking and the Risk of Pancreatic Cancer in the Netherlands Cohort Study

Heinen

Verhage

Goldbohm

et al. 2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

Self Cite

View full text Add to dashboard Cite

Background: To date, cigarette smoking is the most consistent risk factor for pancreatic cancer. We prospectively examined the role of active cigarette smoking, smoking cessation, and passive smoking as determinants for pancreatic cancer.Methods: The Netherlands Cohort Study consisted of 120,852 men and women who completed a baseline questionnaire in 1986. After 16.3 years of follow-up, 520 incident pancreatic cancer cases were available for analysis. A case-cohort approach was employed using the person-years of follow-up of a random subcohort (n = 5,000), which was chosen immediately after baseline.Results: Compared with never cigarette smokers, both former and current cigarette smokers had an increased pancreatic cancer risk [multivariable-adjusted hazard rate ratio (HR), 1.34; 95% confidence interval (CI), 1.02-1.75 and HR, 1.82; 95% CI, 1.40-2.38, respectively]. We observed an increased pancreatic cancer risk per increment of 10 years of smoking (HR, 1.15; 95% CI, 1.08-1.22) and an HR of 1.08 per increment of 10 cigarettes/d (95% CI, 0.98-1.19). Quitting smoking gradually reduced pancreatic cancer risk and approached unity after ≥20 years of quitting. No association was observed for passive smoking exposure and pancreatic cancer risk in women; in men, this association was not investigated because >90% of the men were ever smokers.Conclusions: Overall, our findings confirmed that cigarette smoking is an important risk factor for pancreatic cancer, whereas quitting smoking reduced risk. No association was observed between passive smoking exposure and pancreatic cancer risk in women.Impact: Quitting smoking would benefit the burden on pancreatic cancer incidence. Cancer Epidemiol

show abstract

Cigarette Smoking and Colorectal Cancer: APC Mutations, hMLH1 Expression, and GSTM1 and GSTT1 Polymorphisms

Cited by 54 publications

References 29 publications

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

Morbidity and mortality in relation to smoking among women and men of Chinese ethnicity: The Singapore Chinese Health Study

Active and Passive Smoking and the Risk of Pancreatic Cancer in the Netherlands Cohort Study

Contact Info

Product

Resources

About