Yilmaz, SenayDemirci, Nilgun YilmazMetintas, SelmaZamani, AdilKabalak, Pinar AkinYilmaz, UlkuAk, GuntuluKizilgoz, DeryaOzturk, AkinYilmaz, UfukBatum, OzgurKavas, MuratSerifoglu, IremUnsal, MeftunKomurcuoglu, Berna E.Cengiz, Tuba InalUlubay, GayeOzdemirel, Tugce S.Ozyurek, Berna A.Kavurgaci, SunaAlizoroglu, DursunCelik, PinarErdogan, YurdanurIn, ErdalAksoy, AsudeAltin, SedatGunluoglu, GulsahMetintas, Muzaffer2024-06-282024-06-282021-03-011076-2752https://doi.org/10.1097/JOM.0000000000002115https://hdl.handle.net/11452/42566Objective: 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.eninfo:eu-repo/semantics/closedAccessAnaplastic lymphoma kinaseFactor receptor-mutationsTargeted therapyCancerAssociationSmokingClassificationEpidemiologyExpressionSocietyAlkAsbestosEgfrGenetic alterationsLung adenocarcinomaRos1Science & technologyLife sciences & biomedicinePublic, environmental & occupational healthPublic, environmental & occupational healthArticle00066371920002123824363310.1097/JOM.0000000000002115