|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Precision medicine trials targeting the epidermal growth factor receptor (EGFR) in glioblastoma patients require selection for EGFR-amplified tumors.
|
31125418 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
However, neither PTEN nor EGFR mutation, which is frequently present in glioblastoma, was detected.
|
30496796 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
According to the prevailing model, NHE9 overexpression leads to an increase in plasma membrane density of epidermal growth factor receptors (EGFRs) which consequently enhances GBM cell proliferation and migration.
|
31532058 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The prognosis value of the risk signature was superior than known clinicopathological features in 1p/19q non-codel gliomas and was also highly associated with the following features: loss of CDKN2A/B copy number in mutant-IDH-astrocytoma; telomerase reverse transcriptase (TERT) promoter mutation, combined chromosome 7 gain/chromosome 10 loss and epidermal growth factor receptor amplification in wild-type-IDH-astrocytoma; classical and mesenchymal subtypes in glioblastoma.
|
31157866 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
For glioblastoma (GBM), the epidermal growth factor receptor (EGFR) gene is the most frequently mutated oncogenic driver and has therefore been considered an attractive target for therapy.
|
31054489 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Here we report efficacy, safety and pharmacokinetics (PK) of depatux-m + temozolomide (TMZ) in patients with EGFR-amplified rGBM.
|
29982805 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
We aimed to explore the prognostic impact of epidermal growth factor receptor copy number gain (EGFR CN gain), one of the most common genetic alterations in IDH-WT glioma, in young adults with IDH-WT GBM.
|
31542863 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Specifically, targeting cellular pathways frequently altered in glioblastoma, such as the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), the p53 and the retinoblastoma (RB) pathways, or epidermal growth factor receptor (EGFR) gene amplification or mutation, have failed to improve outcome, likely because of redundant compensatory mechanisms, insufficient target coverage related in part to the blood brain barrier, or poor tolerability and safety.
|
31541850 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
EGFR was significantly associated with all glioma and glioblastoma in males only and a female-specific association in TERT, all of which remained nominally significant after conditioning on known risk loci.
|
30124908 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Here, we evaluated the efficacy of pan-EGFR inhibitor afatinib and Temozolomide (TMZ) combination on GBM in vitro and in vivo.
|
31215502 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
MTT method was used to test the cell viability after EGFR-positive glioblastoma cells were treated with indicated drugs; real-time quantitative PCR method was included to detect the TNFα mRNA levels in glioma tissues and cell lines.
|
31565489 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Here, we identified two enhancers (CE1 and CE2) present within the first intron of the <i>EGFR</i> gene in models of glioblastoma (GBM) and head and neck squamous cell carcinoma (HNSCC).
|
31444232 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
We show that certain genes, like survivin and EGFR, are important for GBM survival, while NKCC1, is more crucial for cancer cell migration.
|
31026613 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Therefore, we performed this study to clarify the importance of EVI1 in GBM by focusing on the regulatory mechanism between EVI1 and EGFR transcription.
|
31617054 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Four genes that were commonly altered in both primary and recurrent GBM were more prevalent in our cohort than reported in COSMIC: CDKN2A (86% vs. 53%) and CDKN2B (86% vs. 54%) deletions, EGFR activating mutation (52% vs. 10%) or amplification (81% vs. 45%), and TERT mutation (95% vs. 51%).
|
30535594 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
In addition, we found that specific FOXO3a activation recapitulated the molecular effects of EGFR inhibition, and that the FOXO3a activator trifluoperazine, a FDA-approved antipsychotic agent, reduced GBM cell growth.
|
30980364 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
In both TCGA database and our clinical data, GBM tissues exhibited increased mRNA expression of GBP1 gene, its expression level was co-related to PETN deletion and EGFR amplification, and was associated with prognosis of GBM patients.
|
29991124 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
These data provide early evidence that combining HDAC and EGFR inhibition may be an effective strategy to reduce GBM growth, through a mechanism possibly involving STAT3.
|
30887411 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
They find that ELOVL2 products help maintain cell membrane organization and EGFR signaling in GSCs, and that targeting PUFA metabolism along with EGFR offers a potential novel therapeutic strategy for glioblastoma.<i>See related article by Gimple et al., p. 1248</i>.
|
31481405 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Macropinocytosis may be notably triggered by epidermal growth factor receptor (EGFR) and platelet-derived growth factor receptor (PDGFR), two well-known markers for glioblastoma aggressiveness.
|
30909495 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
As therapeutic decisions are increasingly guided by biomarkers, and EGFR abnormalities are common in GBM, thus representing a potential therapeutic target, we systematically evaluated methods of assessing <i>EGFR</i> amplification by multiple assays.
|
30796037 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
EGFR gene amplification and classical subtype by TCGA analysis are associated with significantly shorter time to progression for patients with recurrent GBM when treated with bevacizumab.
|
30680510 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
EGFRvIII-specific CAR-T cells were unable to completely treat tumors with heterogenous EGFRvIII expression, leading to outgrowth of EGFRvIII-negative, EGFR-positive glioblastoma.
|
31332324 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
High levels of NO66 in glioma and glioblastoma tissues predict poor patient prognosis, and NO66 is required for EGFR expression and glioblastoma cell proliferation.
|
31704826 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The IC<sub>50</sub> values ranged from 17.34 µg/mL (towards U87MG.ΔEGFR glioblastoma cells) to 40.68 µg/mL (against CCRF-CEM leukemia cells) for FTB, from 16.78 µg/mL (towards U87.
|
30703492 |
2019 |