Clínica de Oncología torácica, and Laboratorio de Oncología Experimental, Instituto Nacional de Cancerología, México, DF, México.
J Thorac Oncol. 2012 Aug;7(8):1228-34. doi: 10.1097/JTO.0b013e3182582a93.
Although 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.
A 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.
Of 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).
NSCLC 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.
虽然吸烟是导致非小细胞肺癌（NSCLC）的主要危险因素，但其他因素也与肺癌的发生有关，例如木柴烟雾暴露（WSE）。本文旨在表明，与吸烟有关的肺癌和与 WSE 有关的肺癌具有不同的临床和遗传特征。
对 914 名肺癌患者进行了前瞻性研究；他们于 2007 年至 2010 年在墨西哥国家癌症研究所接受治疗。分析了 WSE 和吸烟与临床特征、突变谱、化疗反应和表皮生长因子受体酪氨酸激酶抑制剂的关系，并计算了总生存率（OS）。该试验在 ClinicalTrials.gov 上注册：NCT01023828。
在所研究的肺癌患者中，95.1%被归类为非小细胞肺癌组织学亚型；58%的患者吸烟，35%有 WSE 背景（12.1%的患者同时暴露于香烟烟雾和木柴烟雾），19.4%的患者没有吸烟背景。WSE 与 NSCLC 和腺癌组织学有关，并且与吸烟患者相比，更常与表皮生长因子受体突变有关（50.0%比 19.4%），而 KRAS 突变在 WSE 患者中较少见（6.7%比吸烟者中 21%）。WSE 患者表皮生长因子受体酪氨酸激酶抑制剂的反应率（39.7%）高于吸烟者（18.8%）。NSCLC 患者 WSE 组的 OS 比吸烟者（13.8 个月）长（22.7 个月）。
与吸烟有关的 NSCLC 患者与具有 WSE 背景的患者在肿瘤组织学、突变谱、反应率和 OS 方面存在差异，表明这两种烟雾暴露方式诱导了不同的致癌机制。
