RESUMEN
Lung cancer is one of the most common cancers worldwide.Although there are gender differences in lung cancer incidence and mortality, the etiology and pathogenesis of lung cancer in women (LCW) have not been well studied.Women are more susceptible than men to the carcinogenic effects of tobacco, with the clearer underlying mechanisms being synergistic effects between estrogen and polycyclic aromatic hydrocarbons (PAHs) found in tobacco compounds, as well as oncogene mutations that induce the expression of metabolic enzymes, leading to enhanced formation of reactive oxygen species and DNA adducts, and consequently, an increase in the incidence of lung cancer.In contrast, in nonsmoking female lung cancer patients, removing tobacco exposure as a factor, estrogen exerts its proliferative capacity through its receptors ERα and ERβ, most notably ERβ, which influence lung carcinogenesis through genomic and nongenomic signaling.Different isoforms of ERβ can promote apoptosis and thus act as tumor suppressors, and the mechanism for the study of this receptor is not fully understood.In nonsmoking women with lung cancer, alterations in signaling pathways, activation of oncogenes with mutations in oncogenes, and overexposure to cooking fumes increase the risk of lung cancer in women.In this review, we describe the pathogenesis of the increased incidence of lung cancer in tobacco-exposed women, as well as possible etiologic factors and describe the pathogenesis of lung cancer in nonsmoking women.