Based on such preclinical evidence, the phase II FAME trial was designed to test the hypothesis that the addition of metformin, with or without cyclic FMD, to standard platinum-based chemotherapy improves the progression-free survival of patients with advanced, LKB-1 inactive lung adenocarcinoma.
This study aimed to detect EGFR gene mutations using next-generation sequencing (NGS) from different types of body fluids from patients with lung adenocarcinoma.
Re-biopsy and large panel NGS revealed an EGFR mutant lung adenocarcinoma with alternating changes in acquired resistance between EGFR and ALK.The total survival time was 73 months.
Mutations in 59 cancer-associated genes and fusions of ALK and ROS1 were analyzed to understand the molecular features of young patients with lung adenocarcinoma.
Then, the single cells of patients with lung adenocarcinoma receiving gefitinib were captured by laser capture microdissection and analyzed by the above methods to identify the intratumoral heterogeneity of the EGFRL858R mutant.
The proposed deep learning system predicts EGFR-mutant of lung adenocarcinomas in CT images noninvasively and automatically, indicating its potential to help clinical decision-making by identifying eligible patients of pulmonary adenocarcinoma for EGFR-targeted therapy.
The analysis of p22<sup>phox</sup> in lung carcinoma tissues could provide new insights into the selection of chemotherapy for the patients with EGFR-TKI resistant LUAD.
This study elucidated the prevalence and prognostic significance of mutations in the epidermal growth factor receptor gene (<i>EGFR</i>) and rearrangements in the anaplastic lymphoma kinase gene (<i>ALK</i>) in patients with surgically resected primary LAC.
Patients with advanced-stage oligometastatic lung adenocarcinoma harboring sensitive mutation of epidermal growth factor receptor (EGFR) who received EGFR-tyrosine kinase inhibitor (TKI) or EGFR-TKI plus LCT were admitted to Shanghai Chest Hospital from January 2010 to December 2016.
While PD-L1+/-IDO1 expression is observed in association with HLA class I expression, cytotoxic T lymphocyte/Th1 microenvironments, EGFR wild-type, and KRAS mutations, isolated IDO1 expression does not demonstrate these associations, suggesting that IDO1 may serve a distinct immunosuppressive role in lung adenocarcinomas.
To identify which proteins are involved in the restoration of this sensitivity and to provide new therapeutic targets for mutant-KRASlung adenocarcinoma, we performed an iTRAQ quantitative proteomic analysis after subcellular fractionation of H358-NSCLC treated with gefitinib and KDACi (TSA/NAM) versus gefitinib alone.
A consecutive series of surgically resected lung adenocarcinomas were collected and profiled using an enrichment strategy to detect nine common oncogenic driver mutations and fusions concerning EGFR, KRAS, HER2, BRAF, MET, ALK, RET, ROS1, and FGFR.
We describe a 52-year-old man with ISCMs secondary to lung adenocarcinoma who acquired the T790M mutation of the epidermal growth factor receptor (EGFR) after previous use of a first-generation EGFR tyrosine kinase inhibitor (TKI); he was successfully treated with osimertinib.
This study aims to determine the association of EGFR/KRAS mutation status with histological subtypes of lung adenocarcinoma (LAC) based on the IASLC/ATS/ERS classification.