New Molecular Insights in Tobacco-Induced Lung Cancer
We know that cigarette smoking is a leading preventable cause of carcinogenesis in lung cancer. Cigarette smoke is a mixture of more than 5000 chemical compounds, among which more than 60 are recognized to have a specific carcinogenic potential. Carcinogens and their metabolites (i.e., N-nitrosamines and polycyclic aromatic hydrocarbons) can activate multiple pathways, contributing to lung cell transformation in different ways. Nicotine, originally thought only to be responsible for tobacco addiction, is also involved in tumor promotion and progression with antiapoptotic and indirect mitogenic properties. Lung nodules are frequent in smokers and can be transformed into malignant tumors depending on persistant smoking status. Even if detailed mechanisms underlying tobacco-induced cancerogenesis are not completely elucitated, this report collects the emergent body of knowledge in order to simplify the extremely complex framework that links smoking exposure to lung cancer.
Environmental risk factors are important in the etiology of lung cancer, the most important of them being tobacco smoking. The International Agency for Research on Cancer (IARC) identified cigarette smoking as the cause of different organ tumor transformations, including cancers of the lungs, respiratory and digestive tracts (oral cavity, larynx, nasal cavity, esophagus and stomach), pancreas, kidney and urinary bladder. Cigarette smoking is the major risk factor for lung cancer in current and former smokers, in synergistic effect with occupational and environmental particulates (asbestos and arsenic), and has been related to certain types of lung neoplasms such as squamous cell carcinoma and small-cell lung cancer (SCLC). Emerging evidence has clarified that several molecular pathways are involved in lung cancerogenesis with significant differences in the profile of oncogenic mutations among never smokers and smokers. As an example, activating mutations of EGFR appear to be more frequent in never smokers, who, therefore, have increased benefit from biologic agents such as gefitinib and erlotinib. Moreover, smoking habit can affect chemotherapy efficacy through long-term alteration in cytochrome P450-mediated metabolism, glucuronidation and protein binding of chemotherapeutic agents. These observations underline the importance of smoking status assessment for correctly tailored and effective therapy.
This special report aims to highlight the different mechanisms of smoking-induced tumorigenesis and the association of smoking with the onset and development of lung cancer.
Abstract and Introduction
Abstract
We know that cigarette smoking is a leading preventable cause of carcinogenesis in lung cancer. Cigarette smoke is a mixture of more than 5000 chemical compounds, among which more than 60 are recognized to have a specific carcinogenic potential. Carcinogens and their metabolites (i.e., N-nitrosamines and polycyclic aromatic hydrocarbons) can activate multiple pathways, contributing to lung cell transformation in different ways. Nicotine, originally thought only to be responsible for tobacco addiction, is also involved in tumor promotion and progression with antiapoptotic and indirect mitogenic properties. Lung nodules are frequent in smokers and can be transformed into malignant tumors depending on persistant smoking status. Even if detailed mechanisms underlying tobacco-induced cancerogenesis are not completely elucitated, this report collects the emergent body of knowledge in order to simplify the extremely complex framework that links smoking exposure to lung cancer.
Introduction
Environmental risk factors are important in the etiology of lung cancer, the most important of them being tobacco smoking. The International Agency for Research on Cancer (IARC) identified cigarette smoking as the cause of different organ tumor transformations, including cancers of the lungs, respiratory and digestive tracts (oral cavity, larynx, nasal cavity, esophagus and stomach), pancreas, kidney and urinary bladder. Cigarette smoking is the major risk factor for lung cancer in current and former smokers, in synergistic effect with occupational and environmental particulates (asbestos and arsenic), and has been related to certain types of lung neoplasms such as squamous cell carcinoma and small-cell lung cancer (SCLC). Emerging evidence has clarified that several molecular pathways are involved in lung cancerogenesis with significant differences in the profile of oncogenic mutations among never smokers and smokers. As an example, activating mutations of EGFR appear to be more frequent in never smokers, who, therefore, have increased benefit from biologic agents such as gefitinib and erlotinib. Moreover, smoking habit can affect chemotherapy efficacy through long-term alteration in cytochrome P450-mediated metabolism, glucuronidation and protein binding of chemotherapeutic agents. These observations underline the importance of smoking status assessment for correctly tailored and effective therapy.
This special report aims to highlight the different mechanisms of smoking-induced tumorigenesis and the association of smoking with the onset and development of lung cancer.
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