• J Thorac Oncol · Aug 2012

    Clinical and pathological characteristics, outcome and mutational profiles regarding non-small-cell lung cancer related to wood-smoke exposure.

    • Oscar Arrieta, Alma D Campos-Parra, Carlos Zuloaga, Alejandro Avilés, Roberto Sánchez-Reyes, María Eugenia Vázquez Manríquez, Emilia Covián-Molina, Luis Martínez-Barrera, Abelardo Meneses, Andrés Cardona, and José R Borbolla-Escoboza.
    • Clínica de Oncología torácica, and Laboratorio de Oncología Experimental, Instituto Nacional de Cancerología, México, DF, México. ogar@unam.mx
    • J Thorac Oncol. 2012 Aug 1;7(8):1228-34.

    HypothesisAlthough smoking is the major risk factor for non-small-cell lung cancer (NSCLC), other factors are also associated with lung carcinogenesis, such as wood-smoke exposure (WSE). This article has been aimed at suggesting that lung cancer related to cigarette smoking and lung cancer related to WSE have different clinical and genetic characteristics.Experimental DesignA cohort of 914 lung cancer patients was prospectively studied; they had been treated at Mexico's National Cancer Institute between 2007 and 2010. The associations of WSE and cigarette smoking with clinical characteristics, mutation profile, response to chemotherapy, and epidermal growth factor receptor tyrosine kinase inhibitors were analyzed, and overall survival (OS) rate was calculated. The trial was registered with ClinicalTrials.gov: NCT01023828.ResultsOf the lung cancer patients studied, 95.1% were classified as coming within the NSCLC histology subtype; 58% of the patients smoked cigarettes, 35% had a background of WSE (exposure to both cigarette smoke and wood smoke was documented in 12.1% of all patients), and 19.4% patients had no smoke-exposure background. WSE was associated with NSCLC and adenocarcinoma histology, and was also more frequently associated with epidermal growth factor receptor-mutations than cigarette-smoking patients were (50.0% cf. 19.4%), whereas KRAS mutations were less common in WSE patients (6.7%) than in smokers (21%). WSE patients had a higher epidermal growth factor receptor tyrosine kinase inhibitor response rate (39.7%) than smokers (18.8%). The NSCLC patient WSE group's OS was longer (22.7 months) than that for smokers (13.8 months).ConclusionNSCLC patients who smoked tobacco/cigarettes differed from those having a background of WSE regarding tumor histology, mutation profile, response rate, and OS, indicating that different carcinogenic mechanisms were induced by these two types of smoke exposure.

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