Yilmaz, SDemirci, NYMetintas, SZamani, AKaradag, MGuçlu, OAKabalak, PAYilmaz, UAk, GKizilgoz, DOzturk, AYilmaz, UBatum, OKavas, MSerifoglu, IUnsal, MKomurcuoglu, BECengiz, TIUlubay, GOzdemirel, TSOzyurek, BAKavurgaci, SAlizoroglu, DCelik, PErdogan, YIn, EAksoy, AAltin, SGunluoglu, GMetintas, M2024-07-182024-07-181076-27521536-5948http://akademikarsiv.cbu.edu.tr:4000/handle/123456789/10640Objective: 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.EnglishANAPLASTIC LYMPHOMA KINASEFACTOR RECEPTOR-MUTATIONSTARGETED THERAPYCANCERASSOCIATIONSMOKINGCLASSIFICATIONEPIDEMIOLOGYEXPRESSIONSOCIETYArticle