|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
PDGFR alpha expression was related to tumour location and grade and PDGFR beta to histological subtype only.
|
7531297 |
1994 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The association of PDGFR-alpha expression with a distinct subset of glioblastomas characterized by loss of heterozygosity 17p further supports the differentiation of these tumors into molecular variants.
|
8548759 |
1996 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Notably, platelet-derived growth factor receptor alpha (PDGFRA) and members of the downstream RAS/mitogen-activated protein kinase (MAPK) signal transduction pathway are upregulated in M+ tumors.
|
11544480 |
2001 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Southern blot and/or differential PCR analyses identified amplification of PDGFRA (4q12), CCND3 (6p21), EGFR (7p12), CDK4 (12q14) and/or MDM2 (12q14.3-q15), and AKT1 (14q32.3) in the respective tumors.
|
12112531 |
2002 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Analysis of genes encoding proteins that may activate the pathway upstream of Pi3k revealed variable fractions of tumors with EGFR amplification (31%), PDGFRA amplification (8%), and IRS2 amplification (2%).
|
14655756 |
2003 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In this study, GISTs from 37 patients enrolled in an European Organisation for Research and Treatment of Cancer (EORTC) phase I/II clinical study of imatinib were examined for mutations of c-KIT/PDGFRA in order to explore whether the mutational status of the tumour predicts the clinical response to therapy.
|
15010069 |
2004 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In this study, a comprehensive KIT and PDGFRA mutational analysis was performed in a group of 28 epithelioid/mixed type tumors, in order to explore whether a specific KIT/PDGFRA mutational status segregates these neoplasms from spindle cell variant GISTs.
|
15154005 |
2004 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The PDGFRA mutations primarily involved exon 18 (N = 15) and included 11 tumors with missense mutation in codon 842 (PDGFRA D842V or D842Y).
|
15223958 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The PDGFRA does not seem to be an alternative pathway to tumour development in phyllodes tumours because neither expression nor activating mutations were noteworthy.
|
15452163 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
All 17 cases with either mutated KIT (n = 15) or PDGFRA (n = 2) were histologically GIST tumors, whereas none of the other histologic types of cancer (n = 316) harbored KIT or PDGFRA mutation.
|
15545668 |
2005 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Both KIT and PDGFRA expression were associated with high tumour grade, high proliferation index and poor patient outcome.
|
15583695 |
2004 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We have investigated the link between single nucleotide polymorphisms (SNPs) within the PDGFRalpha gene promoter and the occurrence of brain tumours (medulloblastomas, supratentorial primitive neuroectodermal tumours (PNETs), ependymal tumours, astrocytomas, oligodendrogliomas, and mixed gliomas).
|
15635072 |
2005 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
One progressive tumor showed acquired PDGFRA -D842V mutation.
|
15685537 |
2005 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
PDGFRalpha gene mutations were recently described in a subset of GISTs and it has been hypothesized that PDGFRalpha-mutated tumours represent a distinctive entity among GISTs.
|
15693889 |
2005 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Patient tumor EGFR and PDGFRA gene amplifications retained in an invasive intracranial xenograft model of glioblastoma multiforme.
|
15831234 |
2005 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
However, our findings suggest that more than one third of GISTs with PDGFRA mutations may respond to imatinib and that mutation screening may be helpful in the management of these tumors.
|
15928335 |
2005 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The c-KIT and the platelet-derived growth factor receptor alpha (PDGFRalpha) have been shown to be important for tumor growth and progression in several soft-tissue sarcomas, including synovial sarcomas (SSs).
|
16106193 |
2005 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Fibroblast growth receptor 1, platelet-derived growth factor receptor-alpha, and epidermal growth factor receptor are all potential entry points to the phosphatidylinositol 3-kinase and mitogen-activated protein kinase intracellular signaling pathways already known to be important for neoplasia.
|
16186508 |
2005 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Further cytogenetic analysis revealed that this tumor had a point mutation (D842V substitution) in exon 18 of the platelet-derived growth factor receptor alpha gene.
|
16332719 |
2005 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In order to assess the role of PDGFRalpha and c-Kit in malignant peripheral nerve sheath tumours (MPNST) we examined human tumours for structural alterations, protein and ligand expression.
|
16357008 |
2006 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We demonstrate that (i) the NF1-related GISTs do not have KIT or PDGFRA mutations, (ii) the molecular event underlying GIST development in this patient group is a somatic inactivation of the wild-type NF1 allele in the tumor and (iii) inactivation of neurofibromin is an alternate mechanism to (hyper) activate the MAP-kinase pathway, while the JAK-STAT3 and PI3K-AKT pathways are less activated in NF1-related GIST compared with sporadic GISTs.
|
16461335 |
2006 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Pre-treatment samples of GISTs from 377 patients enrolled in phase III study were analyzed for mutations of KIT or PDGFRA by combination of D-HPLC and direct sequencing of tumour genomic DNA.
|
16624552 |
2006 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Thus, lack of mutations in KIT or PDGFRA in solid-pseudopapillary neoplasms suggests that imatinib mesylate is less likely to be effective in the treatment for patients with metastatic disease or unresectable tumor, and patients who are just not good surgical candidates.
|
16778826 |
2006 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In tumor stroma PDGFRalpha was expressed in 35%, PDGFRbeta in 94% and EGFR in 9%.
|
17047316 |
2006 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Mutation analysis of c-Kit hotspot exons (9, 11, 13 and 17) and PDGFRA hotspot exons (12 and 18) was performed in aspirates of 33 GISTs and 18 non-GIST mesenchymal tumors.
|
17145623 |
2007 |