The aim of this study was to evaluate the concordance of EGFR mutation detection between paired primary or recurrent samples, and cerebrospinal fluid (CSF) cytology samples of lung cancer patients.
Here, we demonstrate that apigenin combined with gefitinib inhibits multiple oncogenic drivers such as c-Myc, HIF-1α, and EGFR, reduces Gluts and MCT1 protein expression, and inactivates the 5' adenosine monophosphate-activated protein kinase (AMPK) signaling, which regulates glucose uptake and maintains energy metabolism, leading to impaired energy utilization in EGFRL858R-T790M-mutated H1975 lung cancer cells.
But drastic structural differences can be found between lung cancer and its normal control, including the gain of functional modules for cellular proliferations such as EGFR and PDGFRA, as well as the lost of the important IL6 module, supporting their roles as potential drug targets.
In this study, we evaluated the epidermal growth factor receptor (EGFR) mutation status of samples of lung cancer patients stored before introduction of the plasma EGFR test at our institution.
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.
The identification of activating mutations in the epidermal growth factor receptor (EGFR) gene (deletions in exon 19 [Del19] and point mutation L858R in exon 21) has been the first important step toward molecularly guided precision therapy in lung cancer.
Correction: Monitoring <i>EGFR</i>-T790M mutation in serum/plasma for prediction of response to third-generation EGFR inhibitors in patients with lung cancer.
The targeting therapy of EGFR signaling pathway in non-small cell lung cancer (NSCLC) has achieved a certain effect, but the two mutation of EGFR and other mechanisms of lung cancer resistance still greatly reduce the therapeutic effect of chemotherapy on it.
Further, clinical analysis showed that STC2 expression was increased after the development of EGFR TKI resistance and that higher levels were correlated with shorter progression-free survival in EGFR TKI-treated lung cancer patients.
Functional analysis of the five genes and their protein-protein interaction partners indicated that they are functionally enriched in cell cycle, endocytosis, and EGFR regulation, which are biological processes associated with lung cancer and drug resistance.
The V370D mutation abrogated HGF-dependent drug resistance of lung cancer cells to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI).
Therefore, this paper describes a retrospective study which was conducted to understand the clinicopathologic characteristics and epidermal growth factor receptor (EGFR) mutations in these young lung cancer patients.
To inhibit EGFR-mediated signals, multiple EGFR tyrosine kinase inhibitors (EGFR-TKI) have been developed; however, approximately one third of patients with <i>EGFR</i>-mutated lung cancer do not respond to EGFR-TKIs.
In mutant-EGFR-driven lung cancer, MuSyC reveals that combining a mutant-EGFR inhibitor with inhibitors of other kinases may result only in synergistic potency, whereas synergistic efficacy can be achieved by co-targeting mutant-EGFR and epigenetic regulation or microtubule polymerization.
Repeat percutaneous transthoracic needle aspirations and biopsies for postprogression molecular profiling of epidermal growth factor receptor (<i>EGFR</i>)-mutant lung cancer are safe in everday clinical practice.
It is unknown whether tyrosine kinase inhibitors targeting epidermal growth factor receptor (EGFR) can be discontinued in patients in whom <i>EGFR</i>-mutated lung cancer has well stabilised.
Distribution of EGFR SNPs -191C/A and 181946G/A in patients with lung cancer depending on smoking status in the Republic of Srpska, Bosnia and Herzegovina.