We found a panel of benzisoselenazolones (BISAs) obtained by introducing isothiourea, tetramethylthiourea and heterocyclic groups into the C-ring of Ebselen, including <b>7a</b>, <b>7b</b>, <b>8a</b>, <b>8b</b> and <b>12c</b> (with IC<sub>50</sub> values of less than 20 μM in MET gene amplified lung cancer cell line EBC-1), exhibited more potent antitumour activity than Ebselen by cell growth assay combined with in vitro biochemical assays.
Among former smokers, 1-MET increase and categories of moderate and high cardiorespiratory fitness were associated with 13% (p=0.016), 51%, and 77% (p-trend=0.015) reductions in lung cancer incidence, respectively.
Further prospective studies with more participants for better understanding of mechanism and effect for HGF and c-MET inhibitors in lung cancer will help us to identify of these biomarkers role for guiding us to sellect individualized itargeted therapies.
It was revealed that LINC00887 interacts with several microRNAs (miRs), which regulates downstream genes such as fibronectin 1, MET proto‑oncogene, receptor tyrosine kinase and mothers against decapentaplegic homolog 4, which are associated with the spread of lung cancer.
A 1-MET increase and categories of moderate and high CRF were associated with 10%, 47% and 65% reduction in lung cancer incidence (p=0.002), and 13%, 58% and 76% reduction in cancer mortality (p=0.002), respectively.
Here, we report the dysregulation of mutant MET originally found in a lung cancer patient with Val370 to Asp370 (V370D) replacement located in the extracellular SEMA domain.
This study provides preclinical evidences that combination therapy of CsA and crizotinib is a promising approach for targeted treatment of MET-amplified lung cancer patients.
The presence of MET exon 14 mutations in minor histological types of lung cancers urge to extend screening scope of this mutation in lung cancer and treatment response evaluation in clinical trials.
The cytotoxicity assay results revealed that c‑MET‑CAR‑NK cells exhibited more specific cytotoxicity for HepG2 cells with high c‑MET expression compared with the lung cancer cell line H1299, which has low levels of c‑MET expression.
A significant positive correlation between MET and PD-L1 expression in lung cancer was determined in an analysis based on The Cancer Genome Atlas (TCGA) and in an immunohistochemistry study.
Sarcomatoid transformation is a type of lung cancer histologic evolution with a poor prognosis and a high proportion of cases with aberrant MET activation and PD-L1 expression.
Immunohistochemical analysis of 72 NSCLC patients showed that TIGAR and Met protein expression was positively correlated with late stages of lung cancer.
These findings suggest that cigarette smoke augments oncogene addiction to c-MET in NSCLC cells and that MET inhibitors may show clinical benefits for lung cancer patients with a smoking history.
This unique c-Met targeting aptamer enabled simultaneous monitoring of c-Met on the cell surface with ThT and photodynamic killing of these lung cancer cells with TMPyP4.