|
Non-Small Cell Lung Carcinoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
We found that COX2 and TOPK were highly expressed in EGFR-activating mutated NSCLC and the progression-free survival (PFS) of triple-positive (COX2, MET, and TOPK) patients was shorter than that of triple-negative patients.
|
31611604 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Some patients suffering from non-small cell lung cancer (NSCLC) have difficulty in treating the cancer due to resistance acquired to gefitinib with MET amplification.
|
31323446 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
MET exon 14 skipping is a rare mutation typically found in older, female, and non-smoking patients with NSCLC.
|
30600919 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
We conducted a multicenter retrospective analysis of patients with METex14 NSCLC to determine if treatment with MET inhibitors impacts median overall survival (mOS).
|
31200835 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Therefore, combinatorial therapy with osimertinib and a MET or even a MEK inhibitor should be considered for these patients with resistant NSCLC carrying MET amplification and/or protein hyperactivation.
|
31227004 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
The c-Met receptor is a therapeutically actionable target in non-small-cell lung cancer (NSCLC), with one approved drug and several agents in development.
|
31817278 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
This study examined the antitumor effect of ganetespib in EGFR-mutant non-small cell lung cancer (NSCLC) cells and experimentally established EGFR-tyrosine kinase inhibitor (TKI)-resistant cells harboring various resistance mechanisms, including EGFR T790M mutation, met proto-oncogene amplification, and epithelial-mesenchymal transition.
|
30952716 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Our studies propose that the regulatory mechanisms of the HGF/MET-induced cascade pathway is mediated by FOSL2 in NSCLC metastasis and suggested that FOSL2 could potentially be employed as a prognostic biomarker and potential therapeutic target of NSCLC metastasis.
|
31807006 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Together, these results reveal that the stress hormone NE accelerates Afatinib resistance by increasing the expression of Cx32, which augments MET and IGF-1R levels in cancer cells and provides a promising therapeutic strategy against EGFR-TKI Afatinib resistance in NSCLC.
|
31152452 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
ERBB2 and MET alterations include both activating mutations and gene amplifications, detection of which relies on molecular methods with a minimal role for IHC in NSCLC.
|
30188361 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
ALK and ROS1 are prognostic and predictive tumor markers in non-small cell lung carcinoma (NSCLC), which are more often found in lung adenocarcinomas as with other oncogenes such as EGFR, KRAS, or C-MET.
|
30327151 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
The multi-targeted MET/ALK/ROS1 tyrosine kinase inhibitor (TKI) crizotinib has demonstrated remarkable efficacy in ROS1-rearranged NSCLC.
|
29517860 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
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.
|
29570930 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
MET inhibitors have the potential to benefit subsets of NSCLC patients with specific genetic alterations.
|
29621416 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
In conclusion, this meta-analysis indicates that high MET CNG is an adverse prognostic factor in patients with NSCLC.
|
29805710 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
This phase Ib/II study investigated the safety and efficacy of capmatinib plus gefitinib in patients with EGFR-mutated, MET-dysregulated (amplified/overexpressing) NSCLC who experienced disease progression while receiving EGFR-TKI treatment.
|
30156984 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
EGFR T790M and amplification of c-MET form the two key components of resistant NSCLC.
|
29758406 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Levels of IP3R3 were significantly reduced in both cells and tumors after treatment with crizotinib, whereas EGFR inhibitors caused a reduction of IP3R3 interaction with K-Ras mainly through dephosphorylation of serine residues of K-Ras.<b>Conclusions:</b> Our findings indicate that <sup>18</sup>F-FLT PET/CT is able to detect the enhanced efficacy of EGFR and MET inhibitors in oncogene-driven NSCLC and that such enhancement is mediated by IP3R3 through its interaction with K-Ras.<i></i>.
|
29618618 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Thus, our results highlight a compensatory survival mechanism via the MET/STAT3 signaling pathway after PI3K/AKT signaling inhibition in non-small cell lung cancer.
|
29928341 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Using patient-derived cell line and xenografts, we characterize the mechanism of crizotinib resistance mediated by <i>KRAS</i> amplification in <i>MET</i>ex14-mutant NSCLC and demonstrate the superior efficacy of the dual MET/PI3K inhibition as a therapeutic strategy addressing this resistance mechanism.
|
30072474 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Clinically, EGFR-positive NSCLC acquires several resistance mechanisms during EGFR-TKI treatment, such as the emergence of a secondary mutation (T790M), MET gene amplification, and transformation to small cell lung cancer.
|
30290647 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
In this study, we identified MET exon 14 mutations in 9 (2.0%) of 461 NSCLCs.
|
29338938 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Correlation among genetic variations of c-MET in Chinese patients with non-small cell lung cancer.
|
29416799 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Considered together, the present study has uncovered a novel mechanism underlying mitochondrial regulation by MET that involves crosstalk with DRP1, and suggests that a combination therapy targeting both MET and DRP1 could be a novel strategy for NSCLC and MPM.
|
30311833 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Several clinical studies have highlighted ROS1 as a promising therapeutic target because crizotinib, a multi-targeted drug against ROS1, ALK, and the MET proto-oncogene, has elicited remarkable responses in ROS1-rearrangements NSCLC.
|
29738763 |
2018 |