Lung cancer is one of the leading cause of cancer death worldwide, the most common histological type of lung cancer is non-small cell lung cancer (NSCLC), whose occurrence and development is closely related to the mutation and amplification of epidermal growth factor receptors (EGFR).
Although the EGF receptor tyrosine kinase inhibitors (EGFR-TKI) erlotinib and gefitinib have shown dramatic effects against EGFR mutant lung cancer, patients become resistant by various mechanisms, including gatekeeper EGFR-T790M mutation, Met amplification, and HGF overexpression, thereafter relapsing.
Epidermal growth factor (EGF)/DNA complexes targeted to cancer cells overexpressing the EGF receptor resulted in efficient transduction of several lung cancer cell lines in vitro.
Treatment strategies for non-small-cell lung cancer, the most common form of lung cancer, continue to evolve, most recently with the positive trial results for EGF receptor (EGFR) tyrosine kinase inhibitors in the first-line setting in molecularly targeted populations.
In the present study, we assessed the diagnostic value of epidermal growth factor (egf) and cancer antigens 125 (ca125) and 15-3 (ca15-3) in bronchoalveolar lavage fluid (balf) of lung cancer from 79 enrolled patients with suspected lung cancer.
Stimulation of lung cancer cells with epidermal growth factor activated the signal transducer and activator of transcription 3 pathway and induced expression of Cten in all cell lines.
Patients with advanced or metastatic forms of lung cancer with an activating mutation in <i>epidermal growth factor receptor</i> (<i>EGFR</i>) are given tyrosine kinase inhibitors (TKIs) targeted therapies that are more efficient than chemotherapy.
We investigated the time-dependent PIAS3 shuffling and binding to STAT3 in an EGF-dependent model in lung cancer by using confocal microscopy, immunoprecipitation, luciferase reporter assay, and protein analysis of segregated cellular components.
As both lesions were resected, were of the same histologic subtype and presented the same immunohistochemistry profile; we decided to perform mutational analysis of the epidermal growth factor (EGFR) gene to differentiate between recurrence and second primary lung cancer.
In particular, expression of BCR, which is required for EGFR protein degradation, was induced by EGF stimulation, suggesting a negative feedback loop in lung cancer.
Since a high percentage of lung adenocarcinoma in Asian female nonsmokers contains activating hotspot mutations in epidermal growth factor receptors (EGFR), we hypothesized that NAT2 polymorphisms might represent a risk factor in lung cancer with EGFR mutations.
In this proof-of-concept study, we report wide-field Raman detection of lung cancer using multimodal SERS nanoprobes specific to the EGF receptor family, both in vitro and in vivo.
The role of EGF receptor (EGFR) inhibitors in the treatment of lung cancer without activating EGFR mutations has been a controversial issue, particularly their relative efficacy over the available chemotherapy in the second- and third-line setting.
Pretreatment of A549 lung cancer and JygMC(A) triple-negative breast cancer cells with rhTIMP-2-6XHis in low-nanomolar amounts inhibited EGF-induced proliferation to basal (unstimulated) levels.
Collectively, our in vivo and in vitro findings support that TWIST1 collaborates with the EGF pathway in promoting EMT in EGFR mutated lung adenocarcinoma and that large series of EGFR mutated lung cancer patients are needed to further define the prognostic role of TWIST1 reactivation in this subgroup.
Serum concentrations of Epidermal Growth Factor, sCD26, Calprotectin, Matrix Metalloproteinases -1, -7, -9, CEA and CYFRA 21.1 were determined in 140 patients with respiratory symptoms (lung cancer and controls with/without benign pathology).