Abstract
BackgroundTobacco-smoke is the major etiological factor related to lung cancer. However, other important factor is chronic wood smoke exposure (WSE). Approximately 30 % of lung cancer patients in Mexico have a history of WSE, and present different clinical, pathological and molecular characteristics compared to tobacco related lung cancer, including differences in mutational profiles. There are several molecular alterations identified in WSE associated lung cancer, however most studies have focused on the analysis of changes in several pathogenesis related proteins.MethodsOur group evaluated gene expression profiles of primary lung adenocarcinoma, from patients with history of WSE or tobacco exposure. Differential expression between these two groups were studied through gene expression microarrays.ResultsResults of the gene expression profiling revealed 57 statistically significant genes (p < 0.01). The associated biological functional pathways included: lipid metabolism, biochemistry of small molecules, molecular transport, cell morphology, function and maintenance. A highlight of our analysis is that three of the main functional networks represent 37 differentially expressed genes out of the 57 found. These hubs are related with ubiquitin C, GABA(A) receptor-associated like protein; and the PI3K/AKT and MEK/ERK signaling pathways.ConclusionOur results reflect the intrinsic biology that sustains the development of adenocarcinoma related to WSE and show that there is a different gene expression profile of WSE associated lung adenocarcinoma compared to tobacco exposure, suggesting that they arise through different carcinogenic mechanisms, which may explain the clinical and mutation profile divergences between both lung adenocarcinomas.
Highlights
Tobacco-smoke is the major etiological factor related to lung cancer
We have further described that wood smoke exposure (WSE) related lung cancer is associated with an older age at diagnosis, adenocarcinoma histology, pleural effusion, high prevalence of epidermal growth factor receptor (EGFR) mutations (55.4 %) and a low prevalence of KRAS mutation (6 %), compared to patients with smoking history [15]
Clinical and molecular results The clinical characteristics of the 27 patients included in the microarray analysis are: mean age 62.9 ± 11.7 years, 55.6 % (15/27) were females, WSE was present on 55.6 % of patients (15/27) and 44.4 % (12/27) had tobacco exposure (Table 1)
Summary
Tobacco-smoke is the major etiological factor related to lung cancer. Other important factor is chronic wood smoke exposure (WSE). 30 % of lung cancer patients in Mexico have a history of WSE, and present different clinical, pathological and molecular characteristics compared to tobacco related lung cancer, including differences in mutational profiles. There are several molecular alterations identified in WSE associated lung cancer, most studies have focused on the analysis of changes in several pathogenesis related proteins. Innovations, and progress in diagnosis and treatment, 5-year overall survival is approximately 15 % with high mortality rates [2]. In Mexico, the crude mortality rate of lung cancer is 6.68 per 105 individuals, representing nearly 9000 cases per year, most of them presenting metastatic stage at diagnosis [4, 5]
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