- Author:
Jing WEN
1
;
Jian-Hua FU
;
Wei ZHANG
;
Ming GUO
Author Information
- Publication Type:Journal Article
- MeSH: Adenocarcinoma; etiology; metabolism; pathology; Carcinoma, Squamous Cell; etiology; metabolism; pathology; Humans; Lung Neoplasms; etiology; metabolism; pathology; NF-kappa B; metabolism; Receptor, Epidermal Growth Factor; metabolism; Receptors, Adrenergic, beta; metabolism; Receptors, Nicotinic; metabolism; Signal Transduction; Small Cell Lung Carcinoma; etiology; metabolism; pathology; Smoking; adverse effects; gamma-Aminobutyric Acid; metabolism
- From:Chinese Journal of Cancer 2011;30(8):551-558
- CountryChina
- Language:English
- Abstract: Lung cancer is the leading cause of cancer death in men and women worldwide, with over a million deaths annually. Tobacco smoke is the major etiologic risk factor for lung cancer in current or previous smokers and has been strongly related to certain types of lung cancer, such as small cell lung carcinoma and squamous cell lung carcinoma. In recent years, there has been an increased incidence of lung adenocarcinoma. This change is strongly associated with changes in smoking behavior and cigarette design. Carcinogens present in tobacco products and their intermediate metabolites can activate multiple signaling pathways that contribute to lung cancer carcinogenesis. In this review, we summarize the smoking-activated signaling pathways involved in lung cancer.