Evidence map›Paper›PMID 33099473›Full record

ArticleCancer genomics & proteomics

The KDR (VEGFR-2) Genetic Polymorphism Q472H and c-KIT Polymorphism M541L Are Associated With More Aggressive Behaviour in Astrocytic Gliomas.

Niyaz Zaman, Serena Santhana Dass, Persephone DU Parcq, Suzanne Macmahon, Lewis Gallagher, Lisa Thompson, Jamshid S Khorashad, Clara LimbÄck-Stanic

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Niyaz ZamanDivision of Brain Sciences, Department of Medicine, Imperial College London, London, U.K.
Serena Santhana DassDivision of Brain Sciences, Department of Medicine, Imperial College London, London, U.K.
Persephone DU ParcqDepartment of Cell Pathology, Imperial College Healthcare NHS Trust, London, U.K.
Suzanne MacmahonClinical Genomics, The Centre for Molecular Pathology, The Royal Marsden NHS Foundation Trust, London, U.K.
Lewis GallagherClinical Genomics, The Centre for Molecular Pathology, The Royal Marsden NHS Foundation Trust, London, U.K.
Lisa ThompsonClinical Genomics, The Centre for Molecular Pathology, The Royal Marsden NHS Foundation Trust, London, U.K.
Jamshid S KhorashadDepartment of Immunology and Inflammation, Imperial College London, London, U.K.
Clara LimbÄck-StanicDivision of Brain Sciences, Department of Medicine, Imperial College London, London, U.K. climback@ic.ac.uk.
Imperial College London · GBRoyal Marsden NHS Foundation Trust · GBImperial College Healthcare NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimBetter diagnostic and prognostic markers are required for a more accurate diagnosis and an earlier detection of glioma progression and for suggesting better treatment strategies. This retrospective study aimed to identify actionable gene variants to define potential markers of clinical significance. MATERIALS AND

methods56 glioblastomas (GBM) and 44 grade 2-3 astrocytomas were profiled with next generation sequencing (NGS) as part of routine diagnostic workup and bioinformatics analysis was used for the identification of variants. CD34 immunohistochemistry (IHC) was used to measure microvessel density (MVD) and Log-rank test to compare survival and progression in the presence or absence of these variants.

resultsBioinformatic analysis highlighted frequently occurring variants in genes involved in angiogenesis regulation (KDR, KIT, TP53 and PIK3CA), with the most common ones being KDR (rs1870377) and KIT (rs3822214). The KDR variant was associated with increased MVD and shorter survival in GBM. We did not observe any correlation between the KIT variant and MVD; however, there was an association with tumour grade.

conclusionThis study highlights the role of single-nucleotide variants (SNVs) that may be considered non-pathogenic and suggests the prognostic significance for survival of KIT rs3822214 and KDR rs1870377 and potential importance in planning new treatment strategies for gliomas.

Indexed as

Polymorphism, Single NucleotideAstrocytomaBiomarkers, TumorBrain NeoplasmsFemaleFollow-Up StudiesHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedPrognosisProto-Oncogene Proteins c-kitRetrospective StudiesSurvival RateVascular Endothelial Growth Factor Receptor-2Biomarkers, TumorKDR protein, humanKIT protein, humanProto-Oncogene Proteins c-kitVascular Endothelial Growth Factor Receptor-2artificial intelligenceGliomaKDRKITmicrovascular proliferationnext-generation sequencingpolymorphism

Identifiers

PMID33099473
PMCPMC7675657
OpenAlexW3093906409

What OpenQuestion holds

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Registered trials

None linked

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.