DNAs from pretreatment tumor biopsy samples and re-biopsy samples were assessed to detect T790M by the Cobas EGFR Mutation Test v2 (Cobas) and for quantitating T790M by droplet digital polymerase chain reaction (ddPCR).
In total, 115 paired primary lung adenocarcinoma and corresponding BM tumors were analyzed for EGFR mutations by Amplification Refractory Mutation System.
The dual receptor targeting and enhanced tumour uptake of [<sup>68</sup>Ga]Ga-NOTA-RGD-GE11 warrant its further investigation for dual integrin α<sub>V</sub>β<sub>3</sub> and EGFR-targeted tumour imaging.
We analyzed 366 EGFR-mutated NSCLC patients of the real-life IFCT Biomarkers France study with available pre-treatment formalin-fixed paraffin-embedded (FFPE) tumor DNA before treatment by first/second-generation EGFR-TKI.
Combined effects of HH and EGFR inhibition using Vismodegib and Erlotinib with or without gemcitabine in metastatic solid tumors were assessed by CT. Another cohort of patients with metastatic PDAC was evaluated by FDG-PET and tumor biopsies-derived biomarkers.
Immunohistochemical analysis revealed that the expression level of phosphorylated IGF1R was higher in the tumor specimen from the EGFR-mutant NSCLC patient with acquired resistance to osimertinib than in the specimen collected prior to the treatment.
We collected data from 320 patients with lung carcinoma, including sex, age, smoking history, serum tumour marker levels, maximum standardized uptake value, pathological results, computed tomography images, and EGFR mutation status.
Compared with EGFR-mutant NSCLC, ROS1-rearranged tumors were more likely to exhibit imaging features of lymphangitic carcinomatosis (ROS1, 42%; EGFR, 12%; P < .01) and less likely to have air bronchograms in the primary tumor (ROS1, 2%; EGFR, 28%; P < .01).
Epidermal growth factor receptor (EGFR) signaling pathway plays a fundamental role in regulating cell proliferation, differentiation, apoptosis, migration, and so on, which are associated with tumor development, including the esophageal squamous cell carcinoma (ESCC).
Phase II Study Evaluating the Mechanisms of Resistance on Tumor Tissue and Liquid Biopsy in Patients With EGFR-mutated Non-pretreated Advanced Lung Cancer Receiving Osimertinib Until and Beyond Radiologic Progression: The MELROSE Trial.
Non-small cell lung cancer (NSCLC), since the recognition of epidermal growth factor receptor (EGFR) mutations that sensitized tumors to EGFR tyrosine kinase inhibitors, has been a poster child for precision oncology in solid tumors.
Taken together, VPS33B as a tumor suppressor is easily dysregulated by chemical carcinogens and it interacts with NESG1 to modulate the EGFR/RAS/ERK/c-Myc/p53/miR-133a-3p feedback loop and thus suppress the malignant phenotype of CRC.
For patients with EGFR-mutation-positive lung adenocarcinoma associated with paraneoplastic membranous nephropathy, erlotinib might serve as a treatment option for both the tumour and the membranous nephropathy.
Several growth related genes such as EGFR and VEGF as well as tumour suppressor genes such as p53 have been implicated in LC pathogenesis and progression.
The association between tumour markers, including SF, CEA, and EGFR mutation, and their impact on the prognosis of patients taking EGFR-TKIs was investigated.