|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Twenty-two percent of advanced HCC harbored potentially druggable genetic alterations, and MET amplification was associated with complete tumor response in patients with advanced HCC treated by a specific MET inhibitor.
|
31206197 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we performed global metabolite screening with metabolite set enrichment coupled with transcriptome and gene set enrichment analysis and proteomic screening, and identified substantial reprogramming of tumor metabolism involving oxidative phosphorylation and fatty acid oxidation (FAO) with substantial accumulation of acyl-carnitines accompanied by an increase of PGC1α in response to genetic (shRNA and CRISPR/Cas9) and pharmacologic (crizotinib) inhibition of c-MET.
|
31694905 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Dual inhibition of angiopoietin-TIE2 and MET alters the tumor microenvironment and prolongs survival in a metastatic model of renal cell carcinoma.
|
31582532 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We previously developed a dual EGFR and cMET inhibitor (N19) that was able to inhibit tumor growth in nonsmall cell lung cancer models resistant to EGFR tyrosine kinase inhibitors (TKI).
|
31584260 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Specifically, RNA sequencing and mass spectrometry analysis of cetuximab-sensitive (Cetux<sup>Sen</sup> ) and cetuximab-resistant (Cetux<sup>Res</sup> ) tumors indicated MET amplification and overexpression in the Cetux<sup>Res</sup> tumor compared to the Cetux<sup>Sen</sup> lesion.
|
30694565 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data support the idea that simultaneous targeting of EGFR and MET could be a promising therapeutic strategy inhibiting not only tumor cell growth but also its metastasis.
|
31649529 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Yet, uncommon glioblastoma subsets may exhibit specific vulnerabilities amenable to targeted interventions, including, but not limited to: high tumor mutational burden, BRAF mutation, neurotrophic tryrosine receptor kinase (NTRK) or fibroblast growth factor receptor (FGFR) gene fusions, and MET gene amplification or fusions.
|
31541850 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In opposition, MET amplifications occur usually in the background of other strong genetic events and therefore MET amplifications should be interpreted in the context of each tumor's genetic background, rather than as an isolated driver event, especially when considering MET-specific treatment options.
|
30459450 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Together, our findings warrant the development of novel CAR-T-cell therapies that incorporate HGF receptor neutralizing antibody to improve therapeutic potency, not only in EWS but also in tumors with aberrant activation of the HGF/c-MET pathway.
|
31621900 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
One of the mechanisms conferring gefitinib resistance to lung adenocarcinoma is the amplification of the MET gene, which is observed in 5-22% of gefitinib-resistant tumors.
|
30824185 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Proteome-based networks distinguish functional protein modules for breast tumor groups, with co-expression of EGFR and MET marking ductal carcinoma in situ regions of normal-like tumors and lending to a more accurate classification of this poorly defined subtype.
|
30962452 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Many meta-analyses have shown that aberrant activation of the MET pathway in tumor tissue, including <i>MET</i> gene overexpression, gene amplification, exon 14 skipping and other activating mutations, is almost invariably associated with shorter survival and poor prognosis.
|
31512514 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
NGS is a new emerging technique, which allows high-throughput coverage of frequently mutated genes, including less common BRAF and MET mutations and alterations in tumour suppressor genes.
|
30636374 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Pre- and post-treatment tumor samples were examined for HER2 expression, and for HER2, epidermal growth factor receptor (EGFR), and hepatocyte growth factor receptor (MET) gene amplification.
|
30348707 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The former also showed an association of MET overexpression in a PD-L1<sup>high</sup> tumor with the decreased expressions of T-cell effector molecules.
|
31480591 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<i>MET</i> exon 14 splice site alterations that cause exon skipping at the mRNA level (<i>MET</i>ex14) are actionable oncogenic drivers amenable to therapy with MET tyrosine kinase inhibitors (TKI); however, secondary resistance eventually arises in most cases while other tumors display primary resistance.
|
30352902 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Karyopherin β1 deletion suppresses tumor growth and metastasis in colorectal cancer (CRC) by reducing MET expression.
|
31629952 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
DYRK1A modulates c-MET in pancreatic ductal adenocarcinoma to drive tumour growth.
|
30343272 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Knockdown of TUG1 through MET downregulation suppressed DLBCL cell proliferation and tumor growth.
|
31338678 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this review, we outline the path of discovery concerning the oncogene addiction concept and focus on the MET receptor tyrosine kinase as a model addicting oncoprotein to further explore potential and pitfalls stemming from the implementation of anticancer strategies targeting tumor dependencies beyond their blending with other therapeutic opportunities.
|
30550851 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Validation with RNA-seq data of blood platelets shows that DDR achieves the superior performance in classification of six different tumor types as well as molecular target statuses (such as MET or HER2-positive, and mutant KRAS, EGFR or PIK3CA) with smaller sets of biomarkers.
|
31752658 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Hepatocyte growth factor (HGF) and its receptor MET are expressed in the salivary glands during developmental stages and tumor formation; however, the function of HGF in injured salivary gland tissues remains unclear.
|
31136962 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This notion highlights that the anti-MET therapy can be effective as the first line of intervention in only a few MET-addicted cases, while it is certainly more relevant to block MET in cases of advanced neoplasia that exploit the activation of the invasive growth program to promote dissemination in other body parts.
|
30813513 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Of all measured druggable tyrosine kinases, MET, AXL, or EGFR were expressed at higher levels in tumors than in normal kidney tissues, although intertumor differences were observed.
|
30881919 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The combination of afatinib and a MET inhibitor induced complete tumor regression in <i>ERBB2</i> and <i>MET</i> coamplified patient-derived xenograft models established from a metastatic lesion progressing on afatinib.
|
30463996 |
2019 |