Childhood Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Targeting PDGFRα-activated glioblastoma through specific inhibition of SHP-2-mediated signaling.
|
31232447 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
It has been shown that the dysregulated receptor tyrosine kinase (RTK, including EGFR, MET, PDGFRα, ect.) signaling pathways have pivotal roles in the progression of gliomas, especially glioblastoma.
|
31221203 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
An RNA Aptamer Targeting the Receptor Tyrosine Kinase PDGFRα Induces Anti-tumor Effects through STAT3 and p53 in Glioblastoma.
|
30594071 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A PDGFRα-driven mouse model of glioblastoma reveals a stathmin1-mediated mechanism of sensitivity to vinblastine.
|
30082792 |
2018 |
Childhood Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
EGFR and PDGFRA co-expression and heterodimerization in glioblastoma tumor sphere lines.
|
28831081 |
2017 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
LTS GB showed frequent chromosomal gains in 4q12 (platelet derived growth factor receptor alpha and KIT) and 12q14.1 (cyclin-dependent kinase 4), and deletion in 19q13.33 (BAX, branched chain amino-acid transaminase 2, and cluster of differentiation 33).
|
27932423 |
2017 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Labeling of PDGFRα in glioblastoma cells and tumor-associated stromal cells was highly variable, with no correlation with PFS.
|
27844311 |
2017 |
Childhood Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Tumor types were characterized by specific broad and focal chromosomal events including focal loss of the INK4A/B locus in glioblastoma and loss of the RB1 gene and amplification of the PDGFRA gene in oligodendrogliomas.
|
27251041 |
2016 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Genomic mapping has driven the classification of glioblastoma into distinct molecular subclasses, but mechanisms that regulate tumor subclass phenotypes are only now emerging.In this issue of Cancer Cell, Lu et al. describe a phenotypic switch from PDGFRA-enriched "proneural" to EGFR-enriched "classical" features in glioblastoma upon ablation of Olig2.
|
27165737 |
2016 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PDGFRα depletion attenuates glioblastoma stem cells features by modulation of STAT3, RB1 and multiple oncogenic signals.
|
27344175 |
2016 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The extrachromosomal nature of ALEMs explains the observed drastic changes in the amounts of mutated oncogenes (like EGFR or PDGFRA) in glioblastoma in response to environmental changes.
|
25471132 |
2014 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PDGFRA amplification is common in pediatric and adult high-grade astrocytomas and identifies a poor prognostic group in IDH1 mutant glioblastoma.
|
23438035 |
2013 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A younger age at diagnosis and better clinical outcome in glioblastoma patients is only seen when PDGFRA and KIT are co-amplified.
|
23990986 |
2013 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Intratumoral heterogeneity of receptor tyrosine kinases EGFR and PDGFRA amplification in glioblastoma defines subpopulations with distinct growth factor response.
|
22323597 |
2012 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, PDGFRA has been recently shown to be rearranged in glioblastoma.
|
23074200 |
2012 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although it is known that oncogenic signaling caused by overexpression of genes such as PDGFRA is responsible for robust glioma growth and cell infiltration, the mechanisms underlying glioblastoma malignancy remain largely elusive.
|
22080864 |
2011 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
No significant difference was observed in the frequency of amplification of these genes in primary and secondary glioblastomas or in glioblastomas with and without IDH1 mutations, suggesting that amplification of PDGFRA, KIT and KDR may be implicated in the pathogenesis of a small fraction of both subtypes of glioblastoma.
|
21382095 |
2011 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PDGFRA(Δ8, 9) mutant was common, being present in 40% of the glioblastoma multiformes (GBMs) with PDGFRA amplification.
|
20889717 |
2010 |
Childhood Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Phosphorylated receptor tyrosine kinase profiling showed a specific activation of platelet-derived growth factor receptor alpha/beta in EGFRvIII-transduced pediatric glioblastoma cells, and targeted coinhibition with erlotinib and imatinib leads to enhanced efficacy in this model.
|
19737945 |
2009 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A common theme in glioblastoma is the amplification of genes that code for growth factor receptors of the protein-tyrosine kinase family (epidermal growth factor receptor, platelet-derived growth factor receptor-alpha, met).
|
7654823 |
1995 |