"EGF receptor gene mutations are common in lung cancers from ""never smokers"" and are associated with sensitivity of tumors to gefitinib and erlotinib."
<b>Background</b>: Afatinib is a second-generation epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) that has been approved by the Food and Drug Administration for the treatment of advanced non-small cell lung cancer (NSCLC) harboring EGFR mutations.
<b>Conclusion</b>: This retrospective analysis demonstrated that performance status (KPS≥70), absence of ECM metastases, administration of local treatment and chemotherapy were associated with superior OS in patients with EGFR-mutant NSCLC who developed BM.
<b>Conclusion:</b> For advanced EGFR-positive NSCLC patients with acquired resistance to EGFR-TKI, subsequent treatment should be personalized according to EGFR-TKI failure modes & EGFR mutation subtypes.
<b>Conclusion:</b> This study indicates that PD-L1-positive or EGFR wild-type advanced NSCLC patients might get potential benefit from PD-1/PD-L1 inhibitors.
<b>Conclusion:</b><sup>18</sup>F-FDG PET/CT metabolic parameters combined with clinicopathological data demonstrated moderate diagnostic efficacy in predicting <i>EGFR</i> mutation status and were associated with prognosis in mutant and wild-type <i>EGFR</i> non-small-cell lung cancer (NSCLC), thus providing a reference for individualized targeted molecular therapy.
<b>Conclusions</b> Weight loss at presentation had a detrimental impact on PFS and OS in EGFR-TKI sensitive mutant advanced NSCLC patients treated with first-line EGFR-TKI.
<b>Conclusions:</b> Maintenance pemetrexed post pemetrexed-platinum chemotherapy fails to improve QOL or time to event outcomes over maintenance erlotinib in EGFR mutation negative NSCLC.
<b>Conclusions:</b> TKI+CHM improved PFS when compared with TKI alone in patients with EGFR mutation-positive advanced non-small-cell lung cancer (NSCLC).
<b>Materials and Methods:</b> Patients that had histologically confirmed NSCLC with EGFR mutation, brain metastases, and received TKI or upfront RT with TKI were included in this study.
<b>Materials and Methods:</b> Patients with stage IIIB/IV EGFR mutant NSCLC who had oligoprogressive disease during the first-line EGFR-TKI therapy from March 2011 to February 2016 were identified.
<b>Patients and methods:</b> A prospective observational cohort study was conducted to evaluate the efficacy and safety of osimertinib in patients with a major <i>EGFR</i> mutation and T790M-positive advanced NSCLC who had disease progression after first-line EGFR-TKI therapy.
<b>Patients and methods:</b> Tissues from 163 NSCLC patients at the Affiliated Hospital of Qingdao University were analyzed by next-generation sequencing (NGS) to determine the mutational status of EGFR and concurrent genetic alterations.
<b>Purpose:</b> About 60% of non-small cell lung cancer (NSCLC) patients develop resistance to targeted epidermal growth factor receptor (EGFR) inhibitor therapy through the <i>EGFR</i> T790M mutation.
<b>Purpose:</b> The <i>BIM</i> deletion polymorphism is associated with apoptosis resistance to EGFR tyrosine kinase inhibitors (EGFR-TKI), such as gefitinib and erlotinib, in non-small cell lung cancer (NSCLC) harboring <i>EGFR</i> mutations.
<b>Purpose:</b><i>MET</i> amplification, responsible for 20% of acquired resistance to EGFR tyrosine kinase inhibitor (TKI) in patients with advanced non-small cell lung cancer (NSCLC), presents an attractive target.
<i>EGFR</i>-dependent (T790M and C797S mutations) and independent (Mesenchymal Epithelial Transition [<i>MET</i>] gene amplification, Kirsten Rat Sarcoma [<i>KRAS</i>], Phosphatidyl-Inositol 4,5-bisphosphate 3-Kinase Catalytic subunit Alpha isoform [<i>PI3KCA</i>], and RAF murine sarcoma viral oncogene homolog B1 [<i>BRAF</i>] gene mutations) mechanisms of resistance to EGFR tyrosine kinase inhibitors (TKIs) have been evaluated in plasma samples from NSCLC patients using highly sensitive methods (i.e., digital droplet PCR, Next Generation Sequencing), allowing for the switch to other therapies.