Evidence map›Paper›PMID 19707201›Full record

ArticleBritish journal of cancer2009

Expression, mutation and copy number analysis of platelet-derived growth factor receptor A (PDGFRA) and its ligand PDGFA in gliomas.

O Martinho, A Longatto-Filho, M B K Lambros, A Martins, C Pinheiro, A Silva, F Pardal, J Amorim, A Mackay, F Milanezi and 6 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 130 citations in OpenAlex.

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  11. Diffuse paediatric cerebellar glioma: two identical imaging phenotypes of an extremely rare entity with disparate pathology.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2023
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  15. si-PDGFROxidative medicine and cellular longevity · 2022
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9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 3 countries.

O MartinhoLife and Health Sciences Research Institute, School of Health Sciences, University of Minho, 4710 Braga, Portugal.
A Longatto-Filho
M B K Lambros
A Martins
C Pinheiro
A Silva
F Pardal
J Amorim
A Mackay
F Milanezi
N Tamber
K Fenwick
A Ashworth
J S Reis-Filho
J M Lopes
R M Reis
Institute of Cancer Research · GBUniversity of Minho · PTHospital de São Marcos · PTBreast Cancer Now · GBInstituto Adolfo Lutz · BRUniversidade do Porto · PT

Funding

Breast Cancer Now BREAST CANCER NOW RESEARCH CENTRE
6 · The paper itself

Abstract

backgroundMalignant gliomas are the most prevalent type of primary brain tumours but the therapeutic armamentarium for these tumours is limited. Platelet-derived growth factor (PDGF) signalling has been shown to be a key regulator of glioma development. Clinical trials evaluating the efficacy of anti-PDGFRA therapies on gliomas are ongoing. In this study, we intended to analyse the expression of PDGFA and its receptor PDGFRA, as well as the underlying genetic (mutations and amplification) mechanisms driving their expression in a large series of human gliomas.

methodsPDGFA and PDGFRA expression was evaluated by immunohistochemistry in a series of 160 gliomas of distinct World Health Organization (WHO) malignancy grade. PDGFRA-activating gene mutations (exons 12, 18 and 23) were assessed in a subset of 86 cases by PCR-single-strand conformational polymorphism (PCR-SSCP), followed by direct sequencing. PDGFRA gene amplification analysis was performed in 57 cases by quantitative real-time PCR (QPCR) and further validated in a subset of cases by chromogenic in situ hybridisation (CISH) and microarray-based comparative genomic hybridisation (aCGH).

resultsPDGFA and PDGFRA expression was found in 81.2% (130 out of 160) and 29.6% (48 out of 160) of gliomas, respectively. Its expression was significantly correlated with histological type of the tumours; however, no significant association between the expression of the ligand and its receptor was observed. The absence of PDGFA expression was significantly associated with the age of patients and with poor prognosis. Although PDGFRA gene-activating mutations were not found, PDGFRA gene amplification was observed in 21.1% (12 out of 57) of gliomas. No association was found between the presence of PDGFRA gene amplification and expression, excepting for grade II diffuse astrocytomas.

conclusionThe concurrent expression of PDGFA and PDGFRA in different subtypes of gliomas, reinforce the recognised significance of this signalling pathway in gliomas. PDGFRA gene amplification rather than gene mutation may be the underlying genetic mechanism driving PDGFRA overexpression in a portion of gliomas. Taken together, our results could provide in the future a molecular basis for PDGFRA-targeted therapies in gliomas.

Indexed as

Gene DosageMutationAdolescentAdultAgedBrain NeoplasmsChildChild, PreschoolFemaleGene AmplificationGliomaHumansMaleMiddle AgedPlatelet-Derived Growth FactorReceptor, Platelet-Derived Growth Factor alphaPlatelet-Derived Growth Factorplatelet-derived growth factor AReceptor, Platelet-Derived Growth Factor alpha

Identifiers

PMID19707201
PMCPMC2743351
OpenAlexW2154974088

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.