| Literature DB >> 29113190 |
Rodryg Ramlau1, Paweł Krawczyk2, Rafał Dziadziuszko3, Izabela Chmielewska2, Janusz Milanowski2, Włodzimierz Olszewski4, Katarzyna Stencel5, Katarzyna Ramlau-Piątek6, Agnieszka Segiet7, Michał Skroński8, Jacek Grudny9, Joanna Chorostowska-Wynimko8.
Abstract
Targeted therapy of non-small cell lung cancer (NSCLC) patients with mutations in the epidermal growth factor receptor (EGFR) gene has been associated with improved prognosis. However, there is a shortage on data from real-world clinical practice in management of EGFR-positive NSCLC patients in Poland. The present study retrospectively analyzed data from the INSIGHT study to evaluate the incidence and clinical management of EGFR-positive NSCLC in Poland. The authors additionally aimed to identify predictors of the EGFR mutation and factors associated with clinical stage of the tumor at diagnosis. Incidence of EGFR mutations was 11.8% and the most common mutations were a deletion on exon 19 and an L858R substitution on exon 21. Mutations were strongly associated with female gender [male vs. female odds ratio (OR): 0.51; P=0.004] and never having smoked (current/past smoker vs. never smoked OR: 0.16; P<0.001), and advanced clinical stage (stage IV vs. stage I/II OR: 2.89; P=0.029). Patients with EGFR mutation were also observed to have a greater propensity to develop bone metastasis (OR: 11.62; P=0.008). Multivariate regression analysis demonstrated that patients with past or current smoking history or a poor performance on the Eastern Cooperative Oncology Group (ECOG) scale were less likely to have the EGFR mutation. Furthermore, EGFR-positive patients with greater ECOG scores and a tumor other than adenocarcinoma or squamous cell carcinoma were more likely to present advanced tumors. Early screening for EGFR mutation and the use of EGFR-targeting therapies as first-line agents may lead to better prognosis and successful clinical management of EGFR-positive NSCLC patients.Entities:
Keywords: EGFR mutation; Poland; non-small cell lung cancer; tyrosine kinase inhibitors
Year: 2017 PMID: 29113190 PMCID: PMC5656037 DOI: 10.3892/ol.2017.6907
Source DB: PubMed Journal: Oncol Lett ISSN: 1792-1074 Impact factor: 2.967