Effect of Asbestos Exposure on the Frequency of EGFR Mutations and ALK/ROS1 Rearrangements in Patients With Lung Adenocarcinoma: A Multicentric Study.

OBJECTIVE: The aim of this study is to investigate the effect of asbestos exposure on cancer-driver mutations. METHODS: Between January 2014 and September 2018, epidermal growth factor receptor (EGFR), anaplastic lymphoma receptor tyrosine kinase (ALK), and c-ros oncogene 1 receptor tyrosine kinase gene (ROS1) alterations, demographic characteristics, asbestos exposure, and asbestos-related radiological findings of 1904 patients with lung adenocarcinoma were recorded. RESULTS: The frequencies of EGFR mutations, ALK, and ROS1 rearrangements were 14.5%, 3.7%, and 0.9%, respectively. The rates of EGFR mutations and ALK rearrangements were more frequent in asbestos exposed non-smokers (48.7% and 9%, respectively). EGFR mutation rate was correlated to female gender and not-smoking, ALK rearrangement rate was correlated to younger age, not-smoking, and a history of asbestos exposure. CONCLUSIONS: The higher rate of ALK rearrangements in asbestos-exposed lung adenocarcinoma cases shows that asbestos exposure may most likely cause genetic alterations that drive pulmonary adenocarcinogenesis.

Mean platelet volume as an inflammatory marker in acute exacerbation of chronic obstructive pulmonary disease.

INTRODUCTION:  Mean platelet volume (MPV) is inversely correlated with inflammation in inflammatory bowel diseases, rheumatoid arthritis, and ankylosing spondylitis as shown in the previous studies. It has been reported that elevated values of MPV are associated with cardiovascular diseases and stable chronic obstructive pulmonary disease (COPD). However, MPV values in acute exacerbation of COPD have not been investigated so far. OBJECTIVES:  This retrospective study was conducted to investigate the relationships between MPV and acute phase reactants and functional parameters during COPD exacerbation. PATIENTS AND METHODS:  The study included 47 patients with COPD with mild to very severe airway obstruction and 40 age­matched healthy subjects. C­reactive protein levels and complete blood count were analyzed and compared in patients during the stable period and during exacerbation of COPD. RESULTS:  MPV values were 9.3 ±1.4 and 8.6 ±1.0 fl during stable period and during acute exacerbation, respectively. Mean MPV values in the control group were 9.3 ±0.8 fl. MPV values were significantly lower in patients during acute exacerbation than in those during the stable period of COPD and in control subjects (both, P <0.001). CONCLUSIONS:  The results suggest that assessment of MPV in COPD exacerbation may indicate systemic inflammation. Thus, MPV may be used as a negative acute­phase reactant in COPD exacerbation.