Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Fishing wild-type sparing inhibitors of proto-oncogene c-met variants in renal cell carcinoma from a curated tyrosine kinase inhibitor pool using analog-sensitive kinase technology.
|
30017898 |
2018 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
C-Met protein levels were increased in 8 of 10 RCC tissue samples compared with their adjacent normal tissue and c-Met expression levels were positively associated with a high nuclear grade (P = 0.008) and pT stage (P = 0.002).
|
28427859 |
2017 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
In our study, we used trebananib, an angiopoietin 1/2 inhibitor and a novel small molecule MET kinase inhibitor in patient derived xenograft (PDX) models of ccRCC.
|
31582532 |
2020 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
In the present study, tissue microarrays containing sunitinib-treated and untreated RCC tissues were stained with MET and AXL antibodies.
|
26364599 |
2016 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, all hereditary and sporadic papillary RCCs with MET proto-oncogene show type 1 histological features.
|
12647800 |
2003 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
We report here two pediatric patients with recurrent metastatic RCC whose tumors expressed MET and were treated with cabozantinib.
|
28417541 |
2017 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Presence of phosphorylated hepatocyte growth factor receptor/c-Met is associated with tumor progression and survival in patients with conventional renal cell carcinoma.
|
16914575 |
2006 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
The significance of ligand-dependent MET activation in RCC bone metastasis is considered, and HAI-2 may be an important regulator in this system.
|
29890660 |
2018 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
CTD_human |
Spectrum of diverse genomic alterations define non-clear cell renal carcinoma subtypes.
|
25401301 |
2015 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
PosttranslationalModification
|
disease |
BEFREE |
Inactivation of von Hippel-Lindau gene induces constitutive phosphorylation of MET protein in clear cell renal carcinoma.
|
16585196 |
2006 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Wilms' tumour and the WT-1 gene, renal cell carcinoma and the c-met receptor tyrosine kinase gene), some to be caused by mutations in genes expressed during normal development (e.g. renal cell carcinoma and the TSC-2 gene, renal cell carcinoma of the clear cell variety and the VHL gene).
|
10535327 |
1999 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Matriptase and MET are prominently expressed at the site of bone metastasis in renal cell carcinoma: immunohistochemical analysis.
|
25186085 |
2015 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Increased cell motility associated with HAI-2/SPINT2 inactivation was abrogated by treatment with extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) and phospholipase C-gamma inhibitors, but not by an inhibitor of atypical protein kinase C. These findings are consistent with frequent epigenetic inactivation of HAI-2/SPINT2, causing loss of RCC tumor suppressor activity and implicate abnormalities of the MET pathway in clear cell and papillary sporadic RCC.
|
15930277 |
2005 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
CausalMutation
|
disease |
CGI |
|
|
|
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Other tyrosine kinases' pathways, including PDGFR, Axl or MET have emerged as key signaling pathways involved in RCC biology.
|
30999623 |
2019 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Mutations of MET also have been identified in a subset of tumors from patients with sporadic type 1 papillary renal cell carcinoma (RCC).
|
19402075 |
2009 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Combination strategies of VEGF and MET inhibitors could lead to sustained and deep responses even in non-MET driven RCC by inhibiting pathways of VEGF resistance.
|
31554440 |
2019 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
The MET gene on chromosome 7, for example, was found to be involved in both forms of papillary RCC.
|
12351585 |
2002 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Renal cell carcinoma (RCC) is a metabolic disease, being characterized by the dysregulation of metabolic pathways involved in oxygen sensing (VHL/HIF pathway alterations and the subsequent up-regulation of HIF-responsive genes such as VEGF, PDGF, EGF, and glucose transporters GLUT1 and GLUT4, which justify the RCC reliance on aerobic glycolysis), energy sensing (fumarate hydratase-deficient, succinate dehydrogenase-deficient RCC, mutations of HGF/MET pathway resulting in the metabolic Warburg shift marked by RCC increased dependence on aerobic glycolysis and the pentose phosphate shunt, augmented lipogenesis, and reduced AMPK and Krebs cycle activity) and/or nutrient sensing cascade (deregulation of AMPK-TSC1/2-mTOR and PI3K-Akt-mTOR pathways).
|
27453294 |
2016 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Cabozantinib is a potent inhibitor of VEGF, AXL and MET receptors providing rationale for its use in RCC.
|
31184937 |
2019 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
For this purpose, tumor samples were analyzed for c-MET expression by immunohistochemistry (IHC), for c-MET copy number alterations by fluorescence in situ hybridization (FISH), and for c-MET mutations by next generation sequencing (NGS) in a retrospective cohort of 90 primary ccRCC of patients with metastases treated by first-line sunitinib.
|
28550387 |
2017 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Studies of the hereditary form of renal cell carcinoma (RCC) associated with hereditary papillary renal carcinoma (HPRC) determined that the c-Met proto-oncogene on chromosome 7 is the gene for HPRC and for a number of sporadic papillary RCCs.
|
15448018 |
2004 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The exonic MET variant rs11762213 is an independent predictor of adverse CSS and TTR in ccRCC and should be integrated into clinical practice for prognostic stratification.
|
26505625 |
2016 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
We examined the gene expression of HGF and MET in 27 primary RCC tumors by quantitative competitive RT-PCR.
|
10022739 |
1999 |
Conventional (Clear Cell) Renal Cell Carcinoma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Mechanistic, preclinical, and early clinical data highlight c-Met / hepatocyte growth factor receptor as a promising target for RCC therapeutic agents.We have examined MET expression, frequency of MET gene copy gains and MET gene mutation in a large, hospital-based series of renal cell carcinomas with long-term follow-up information.Out of a total of 572 clear-cell RCC, only 17% were negative for MET expression whereas 32% showed high protein levels.
|
27894094 |
2017 |