Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF) is a ligand for the EGF receptor (EGFR), one of the most commonly amplified receptor tyrosine kinases (RTKs) in glioblastoma (GBM).
|
28368403 |
2017 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Here we developed a purification strategy to directly isolate EGFR<sup>+/-</sup> populations from human germinal matrix (GM) and adult subventricular zone autopsy tissues, and from de novo glioblastoma (GBM) resections, enriching for cells capable of binding EGF ligand (<sup>LB</sup>EGFR<sup>+</sup>), and uniquely compared their functional and molecular properties.
|
28434940 |
2017 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Here we report the development and selection for a rearranged amplified EGF receptor, which lacks cytoplasmic amino acid sequences in a human glioblastoma xenograft.
|
10411339 |
1999 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Here, we found that expression of EphA3 is up-regulated in response to epidermal growth factor (EGF) stimulation and promotes formation of cell aggregates in suspension culture of glioblastoma cells.
|
30528229 |
2019 |
Glioblastoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Here, we show the first example of this alternate mechanism in brain tumors by showing that EGF receptor (EGFR)-mutant glioblastomas (GBMs) evade EGFR TKIs by transcriptionally de-repressing platelet-derived growth factor receptor β (PDGFRβ).
|
23533263 |
2013 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
High-level EGFR amplification was rapidly lost in 5 glioblastoma cultures supplemented with EGF, whereas it was preserved in cultures from the same tumors established without EGF.
|
22316604 |
2012 |
Glioblastoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Immunohistochemical analysis of the mutant epidermal growth factor, deltaEGFR, in glioblastoma.
|
15700833 |
2004 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
In absence of EGF in the medium, EGFR amplification was more conserved and NFKBIA deletion less frequent point to a low frequency of NFKBIA deletions in GBM and suggest that EGF in the culture medium of NS may affect frequency not only of EGFR amplifications but also of NFKBIA deletions.
|
24330732 |
2013 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
In addition, ectopic expression of α-catenin or depletion of β-catenin suppresses EGF-promoted glioblastoma cell migration, invasion, and proliferation.
|
20872274 |
2011 |
Glioblastoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In analyses of primary GBM tissue and RNA specimens, we found that GRK3 expression is correlated with established criteria for GBM subtyping including expression of EGF receptor, platelet-derived growth factor receptor (PDGFR)α, NF1, PTEN, CDKN2A, and neurofilament.
|
22086906 |
2012 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
In contrast, EGF-induced glioblastoma migration requires both ERK1/2 and PI3K activity.
|
20392929 |
2010 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
In contrast, immunoreactivity for the EGF receptor prevailed in primary glioblastomas (63%) but was rare in secondary glioblastomas (10%).
|
8864278 |
1996 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
In total, these results indicate that the aberrant EGF receptor synthesized in glioblastomas, and which lacks a portion of the extracellular domain necessary for ligand binding, is an activated tyrosine kinase.
|
8036013 |
1994 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
In view of the similarity to the activated viral and cellular erbB genes in the avian system, these mutated and overexpressed EGF receptors might play a role in the onset or development of human glioblastoma cells.
|
3380099 |
1988 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
CTD_human |
Inhibition of matrix degrading enzymes and invasion in human glioblastoma (U87MG) cells by isoflavones.
|
16598420 |
2006 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Kinase-deficient erbB proteins reduced epidermal growth factor (EGF)-induced tyrosine phosphorylation of endogenous Shc proteins and also reduced immediate and sustained EGF-induced ERK MAPK activities in human glioblastoma cells, although basal ERK MAPK activities were unaffected.
|
10541432 |
1999 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Lymphocytes were depleted in the classical transcriptional class and in EGF receptor (EGFR)-amplified and homozygous PTEN-deleted glioblastomas.
|
23864165 |
2013 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Neutralizing the EGF receptor in glioblastoma cells stimulates cell migration by activating uPAR-initiated cell signaling.
|
25347738 |
2015 |
Glioblastoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
No significant association was observed between the EGF+61 polymorphism and glioblastoma or oligodendroglioma patients' overall survival.
|
17473192 |
2007 |
Glioblastoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Particularly salient are the following: (1) gene amplification is related to increasing grade of human glioma malignancy and occurs in approximately 40% of the most common and most malignant variety of glioma, glioblastoma multiforme (GBM), (2) by far the most commonly amplified gene in glioblastomas is the epidermal growth factor receptor (EGFR) gene, which is amplified in about one third of GBMs, (3) a small percentage of GBMs amplify N-myc or the novel sequence gli, (4) the EGFR gene is rearranged in at least half of gliomas in which it is amplified, and (5) EGFR gene rearrangement results in external domain deletions that yield truncated EGF receptors.
|
1374522 |
1992 |
Glioblastoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Polymorphism in Sp1 recognition site of the EGF receptor gene promoter and risk of glioblastoma.
|
16885506 |
2006 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Primary (de novo) glioblastomas develop in older patients and are characterized by epidermal growth factor (EGF) receptor amplification/overexpression, p16 deletion, and PTEN mutations, whereas secondary glioblastomas that progressed from low-grade or anaplastic astrocytoma develop in younger patients and frequently contain p53 mutations.
|
10666371 |
2000 |
Glioblastoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Primary (de novo) glioblastomas are characterized by amplification/overexpression of the EGF receptor (EGFR) and, less frequently, of the MDM2 gene.
|
9370234 |
1997 |
Glioblastoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Resistance to EGF receptor inhibitors in glioblastoma mediated by phosphorylation of the PTEN tumor suppressor at tyrosine 240.
|
22891331 |
2012 |
Glioblastoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Retroviral vectors made with the fusion protein were able to bind peptide antigen and EGFRvIII expressed on the surface of human glioblastoma cells.
|
10725459 |
2000 |