adenoma/نيكوتين

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Association Between Exposure to Environmental Tobacco Smoke at the Workplace and Risk for Developing a Colorectal Adenoma: A Cross-Sectional Study.

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OBJECTIVE A colorectal adenoma (CRA) is a well-defined precursor to colorectal cancer (CRC). Additionally, smoking is a potent risk factor for developing a CRA, as well as CRC. However, the association between exposure to environmental tobacco smoke (ETS) and the risk for developing a CRA has not

Coffee, tobacco and alcohol as risk factors for cancer and adenoma of the large intestine.

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Our aim was to estimate the association between smoking history, alcohol and tobacco smoking and tumours of the large intestine. Associations were studied at an early stage of colorectal cancer in order to avoid bias in the information. In order to estimate the link between adenoma and cancer the

DNA repair gene polymorphisms and tobacco smoking in the risk for colorectal adenomas.

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DNA damage is thought to play a critical role in the development of colorectal adenoma. Variation in DNA repair genes may alter their capacity to correct endogenous and exogenous DNA damage. We explored the association between common single-nucleotide polymorphisms (SNPs) in DNA repair genes and

[Alcohol, tobacco and colorectal adenomas and cancer. Case-control study in a population with positive fecal occult blood tests].

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OBJECTIVE To analyze the associations between lifestyle factors and colorectal adenomas or cancers in a population 50-74 years old. METHODS The study population underwent colonoscopy after positive fecal occult blood test in Health examination centers of the French general health insurance. The two

Tobacco, colorectal cancer, and adenomas: a review of the evidence.

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Although tobacco has been clearly implicated as a cause of a number of cancers, earlier studies had not generally found cigarette smokers to be at higher risk for cancers of the large bowel. Unlike the earlier studies, more recent studies have tended to find cigarette smokers to be at higher risk of

Phenethyl isothiocyanate and sulforaphane and their N-acetylcysteine conjugates inhibit malignant progression of lung adenomas induced by tobacco carcinogens in A/J mice.

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We have shown previously that naturally occurring isothiocyanates derived from cruciferous vegetables and their N-acetylcysteine conjugates inhibit lung adenoma formation induced by tobacco carcinogens in A/J mice at the post-initiation stage. The tumor-inhibitory activity by these compounds is

Tobacco use and associations of beta-carotene and vitamin intakes with colorectal adenoma risk.

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The effects of vitamins and beta-carotene on the risk of colorectal adenomas have not been fully investigated. Recent data suggest that smoking could modulate the effect of beta-carotene supplements on adenoma recurrence. We investigated the effect of dietary vitamins and beta-carotene on the risk

Alcohol and tobacco use: risk factors for colorectal adenoma and carcinoma?

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A prospective study of cigarette smoking and risk of colorectal adenoma and colorectal cancer in U.S. men.

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BACKGROUND Epidemiologic studies of men consistently demonstrate a positive association between tobacco smoking and risk of colorectal adenomas, precursors of cancer, but have not consistently shown an association between smoking and colorectal cancer. We hypothesized that smoking acts as an

A study of tobacco carcinogenesis. XLVII. Bioassays of vinylpyridines for genotoxicity and for tumorigenicity in A/J mice.

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3-Vinylpyridine is formed from nicotine during the smoking of tobacco products. Consequently it is found in mainstream and side-stream smoke of cigarettes and cigars and in environmental tobacco smoke. In this study, 3-vinylpyridine and its isomers 2- and 4-vinylpyridine as well as styrene

Relationship of aging and tobacco use with the development of aberrant crypt foci in a predominantly African-American population.

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OBJECTIVE In clinical studies, diminished folate availability appears to increase the risk for colorectal neoplasms. Additionally, alcohol and tobacco use are associated with an increased risk for colon cancer, but the early pathologic events by which these agents promote neoplastic transformation

Genetic polymorphism of CYP2A6 as one of the potential determinants of tobacco-related cancer risk.

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Analyzing the CYP2A6 gene of subjects who showed a poor metabolic phenotype toward SM-12502, we discovered a novel mutant allele (CYP2A6*4C) lacking the whole CYP2A6 gene. Using genetically engineered Salmonella typhimurium expressing a human CYP, we found that CYP2A6 was involved in the metabolic

The carcinogenicity of environmental tobacco smoke.

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Male strain A/J mice were exposed for 6 h a day, 5 days a week to environmental tobacco smoke (ETS) generated from Kentucky 1R4F reference cigarettes. Chamber concentrations were 87 mg/m3 of total suspended particulate matter (TSP), 246 p.p.m. of CO and 16 mg/m3 of nicotine. After 5 months, 33% of

Tobacco specific N-nitrosamines: occurrence and bioassays.

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A new GC-TEA method for the analysis of tobacco-specific N-nitrosamines (TSNA) has been developed. Four TSNA have thus far been identified; these are N'-nitrosonornicotine (NNN), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), N'-nitrosoanatabine (NAT) and N'-nitrosoanabasine (NAB). The method

Chemical studies on tobacco smoke. XLII. Nitrosonornicotine: presence in tobacco, formation and carcinogenicity.

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NNN is the first organic carcinogen isolated from unburned tobacco. It has been found in smoking tobaccos, chewing tobaccos and in snuff in concentrations between 0.3 and 90.0 mug. This appears to be an unusually high concentration for a nitrosamine in an environmental agent. We have presented data

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