Smoking and lung cancer.

Department of Chest Diseases, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey.
Tuberkuloz ve toraks 02/2005; 53(2):200-9.
Source: PubMed

ABSTRACT Nowadays, around one-third of adults are known to be smokers, and smoking rates are increasing among the female population. It is estimated that deaths attributable to tobacco use will rise to 10 million by 2025, and one-third of all adult deaths are expected to be related to cigarette smoking. The association between cigarettes and lung cancer has been proven by large cohort studies. Tobacco use has been reported to be the main cause of 90% of male and 79% of female lung cancers. 90% of deaths from lung cancer are estimated to be due to smoking. The risk of lung cancer development is 20-40 times higher in lifelong smokers compared to non-smokers. Environmental cigarette smoke exposure and different types of smoking have been shown to cause pulmonary carcinoma. DNA adducts, the metabolites of smoke carcinogens bound covalently with DNA, are regarded as an indicator of cancer risk in smokers. In recent decades, there has been a shift from squamous and small cell lung cancer types to adenocarcinoma, due to increasing rates of smoking among female population and rising light cigarette usage. After smoking cessation, the cumulative death risk from lung cancer decreases. Patients who continue smoking experience greater difficulties during cancer treatment. Stopping smoking may prolong survival in cancer patients, and also decreases the risk of recurrent pulmonary carcinoma. In order to save lives and prevent smoking related hazards, physicians should advise both healthy individuals and those with cancer of the benefits of stopping smoking.

0 0
  • [show abstract] [hide abstract]
    ABSTRACT: The association of two cytochrome P4501A1 (CYP1A1) polymorphisms, m1 (T6235C transition) and m2 (A4889G transition), with gastric cancer risk is inconclusive. We conducted a meta-analysis of all available studies to evaluate the potential role of the polymorphisms and their interactions with tobacco smoking in gastric cancer susceptibility. Published literature from PubMed was retrieved by two investigators independently. Fourteen case-control studies with 2,032 gastric cancer cases and 5,099 controls were selected. A fixed effects model or a random-effects model was used to estimate the odds ratio (OR) for the CYP1A1 polymorphisms and the occurrence of gastric cancer. Significant associations between CYP1A1 m1 and m2 polymorphisms and gastric cancer susceptibility were not observed in all genetic models in the overall analyses. Subgroup analyses by ethnicity and source of controls did not reveal significant associations with gastric cancer risk. Stratification analysis by smoking status found that carriers of the heterozygous and homozygous m1 genotypes decreased the susceptibility of gastric cancer among ever-smokers (pooled OR = 0.56, 95 % CI 0.36-0.89, fixed effects). In contrast, the m2 genotypes (G/G and A/G) did not show any relevance to gastric cancer risk among the smoking population (pooled OR = 1.30, 95 % CI 0.84-2.00, fixed effects). Overall, we found that the CYP1A1 polymorphism itself, either m1 or m2, did not represent an independent genetic risk factor influencing gastric cancer. However, subgroup analyses suggest that carriers of the heterozygous and homozygous m1 genotype who are exposed to tobacco smoke have a significantly lower risk of developing gastric cancer. To explain the observed reduction of gastric cancer risk, we proposed a novel hypothesis of "observation bias". This hypothesis is also applicable to explain the combined effects of other genetic polymorphisms and environmental factors on the risk of developing cancers, and the rationality of the hypothesis needs to be further investigated.
    Molecular Biology Reports 06/2012; 39(8):8335-44. · 2.51 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: The environment and dietary factors play an essential role in the etiology of cancer. Environmental component is implicated in ~80 % of all cancers; however, the causes for certain cancers are still unknown. The potential players associated with various cancers include chemicals, heavy metals, diet, radiation, and smoking. Lifestyle habits such as smoking and alcohol consumption, exposure to certain chemicals (e.g., polycyclic aromatic hydrocarbons, organochlorines), metals and pesticides also pose risk in causing human cancers. Several studies indicated a strong association of lung cancer with the exposure to tobacco products and asbestos. The contribution of excessive sunlight, radiation, occupational exposure (e.g., painting, coal, and certain metals) is also well established in cancer. Smoking, excessive alcohol intake, consumption of an unhealthy diet, and lack of physical activity can act as risk factors for cancer and also impact the prognosis. Even though the environmental disposition is linked to cancer, the level and duration of carcinogen-exposure and associated cellular and biochemical aspects determine the actual risk. Modulations in metabolism and DNA adduct formation are considered central mechanisms in environmental carcinogenesis. This review describes the major environmental contributors in causing cancer with an emphasis on molecular aspects associated with environmental disposition in carcinogenesis.
    Tumor Biology 05/2012; 33(5):1265-74. · 2.52 Impact Factor
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: BACKGROUND: This review summarizes peer-reviewed studies examining cancer risks among police officers. It provides an overview of existing research limitations and uncertainties and the plausible etiologic risk factors associated with cancer in this understudied occupation. METHODS: Previous cancer studies among police officers were obtained via a systematic review of the MEDLINE, CABDirect, and Web of Science bibliographic databases. RESULTS: Quality observational studies of cancer among police officers are sparse and subject to limitations in exposure assessment and other methods. Results from three studies suggested possible increased mortality risks for all cancers, and cancers of the colon, kidney, digestive system, esophagus, male breast, and testis, as well as Hodgkin's disease. Few incidence studies have been performed, and results have been mixed, although some associations with police work have been observed for thyroid, skin, and male breast cancer. CONCLUSIONS: Police are exposed to a mix of known or suspected agents or activities that increase cancer risk. Epidemiologic evidence to date is sparse and inconsistent. There is a critical need for more research to understand the biological and social processes underlying exposures and the suggested disproportionate risks and to identify effective prevention strategies. Am. J. Ind. Med. © 2012 Wiley Periodicals, Inc.
    American Journal of Industrial Medicine 12/2012; · 1.97 Impact Factor