As EGFR-mutated lung cancer favours female, never-smoker, adenocarcinoma and Asians, it may be argued that there may be some underlying genetic modifiers responsible for the pathogenesis of EGFR mutation.
Anaplastic lymphoma kinase (ALK) is a transmembrane receptor tyrosine kinase, and ALK rearrangements are responsible for 3-7% of NSCLC, predominantly of the adenocarcinoma subtype, and occur in a mutually exclusive manner with KRAS and EGFR mutations.
Outcome of EGFR-mutated adenocarcinoma NSCLC patients with changed phenotype to squamous cell carcinoma after tyrosine kinase inhibitors: A pooled analysis with an additional case.
Computed Tomography-Based Radiomics Signature: A Potential Indicator of Epidermal Growth Factor Receptor Mutation in Pulmonary Adenocarcinoma Appearing as a Subsolid Nodule.
Synthesis, Characterization, and Evaluation of Near-IR Boron Dipyrromethene Bioconjugates for Labeling of Adenocarcinomas by Selectively Targeting the Epidermal Growth Factor Receptor.
To investigate the status and distribution of epidermal growth factor receptor (EGFR), hepatocyte growth factor receptor (MET), and receptor tyrosine kinase (ROS1) genes in patients with non-small cell lung (NSCL) adenocarcinoma.
Currently, for patients with advanced adenocarcinomas, testing for sensitizing mutations in epidermal growth factor receptor (EGFR) is mandatory prior to the administration of anti-EGFR inhibitors such as erlotinib, gefitinib, afatinib, or osimertinib.
This study aimed to retrospectively evaluate the efficacy of platinum-based adjuvant chemotherapy (PBAC) for patients with pathological II/III pulmonary adenocarcinoma after curative resection based on epidermal growth factor receptor (EGFR) mutation status using propensity score matching (PSM) analysis.
Alterations characteristic of adenocarcinoma (EGFR, KRAS, ALK receptor tyrosine kinase [ALK], ROS1, and serine/threonine kinase 11 [STK11]) were detected in the LCC-AD subgroup but not in LCC-SqCC, whereas squamous-lineage alterations (phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha [PIK3CA], SRY-box 2 [SOX2], fibroblast growth factor receptor 1 [FGFR1], and AKT1) were detected in the LCC-SqCC subgroup but not in the LCC-AD group.
EGFR mutations were more common in patients with resected lepidic predominant adenocarcinoma (OR,1.76; 95%CI, 1.38-2.24;p < 0.01) and were rarely found in solid predominant adenocarcinoma (OR,0.28; 95%CI, 0.23-0.34;p < 0.01) or IMA (OR,0.10; 95%CI, 0.06-0.14;p < 0.01).
We describe the case of a woman with metastatic lung cancer adenocarcinoma with mutated EGFR with an initial response to gefitinib and radiation therapy, who progressed after 18 months due to the development of a resistance mechanism.
Carnosic Acid, Tangeretin, and Ginkgolide-B Anti-neoplastic Cytotoxicity in Dual Combination with Dexamethasone-[anti-EGFR] in Pulmonary Adenocarcinoma (A549).
After multiple-line treatments, favourable PFS was associated with tumor histological types of adenocarcinoma (P = 0.041), genetic lesions at exon 19 of EGFR (P = 0.001) and fourth-line treatment (P = 0.001).
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.
We assessed whether adding panitumumab (an EGFR inhibitor) or rilotumumab (a HGF inhibitor) to first-line fluoropyrimidine-based and platinum-based chemotherapy (modified oxaliplatin, leucovorin and fluorouracil [mFOLFOX6]) benefits to patients with advanced gastroesophageal adenocarcinoma.
These results support the extended the use of EGFR inhibitors beyond monotherapy in the EGFR-mutated adenocarcinoma setting in combination with FGFR inhibitors for selected patients with increased FGFR1 overexpression and EGFR activation.
In the multivariate analysis, smoking status (never‑smoking), histopathology (adenocarcinoma) and SUVmax (≤9.91) were the statistically significant predictors of EGFR mutations.
Between EGFR mutant and wild-type adenocarcinoma, ROC analysis showed significant difference in 2/11 radiomic features (kurtosis, K2) [AUC 0.656-0.713, P = .03 to .003], 1/3 clinical features (smoking) [AUC 0.758, P < .0001].