Evidence map›Paper›PMID 26179332›Full record

ArticleInternational journal of oncology2015

Vascular endothelial growth factor directly stimulates tumour cell proliferation in non-small cell lung cancer.

Aoife M Devery, Rekha Wadekar, Sivan M Bokobza, Anika M Weber, Yanyan Jiang, Anderson J Ryan

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Vascular endothelial growth factor levels in patients with obstructive sleep apnea: a meta-analysis.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2017
    Pooled it
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  10. Unfolded protein response and angiogenesis in malignancies.Biochimica et biophysica acta. Reviews on cancer · 2023
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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

6 authors at 2 institutions in 1 country.

Aoife M DeveryCRUK and MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Rekha WadekarCRUK and MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Sivan M BokobzaCRUK and MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Anika M WeberCRUK and MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Yanyan JiangCRUK and MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Anderson J RyanCRUK and MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Headington, Oxford OX3 7DQ, UK.
University of Oxford · GBCRUK/MRC Oxford Institute for Radiation Oncology · GB

Funding

Medical Research Council MC_PC_12006
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) is a key stimulator of physiological and pathological angiogenesis. VEGF signals primarily through VEGF receptor 2 (VEGFR2), a receptor tyrosine kinase whose expression is found predominantly on endothelial cells. The purpose of this study was to determine the role of VEGFR2 expression in NSCLC cells. NSCLC cells and tissue sections were stained for VEGFR2 expression by immunohistochemistry (IHC). Immunoblotting and ELISA were used to determine the activation and inhibition of VEGFR2 and its downstream signalling pathways. Five-day proliferation assays were carried out in the presence or absence of VEGF. IHC analysis of NSCLC demonstrated tumour cell VEGFR2 expression in 20% of samples. Immunoblot analysis showed expression of VEGFR2 protein in 3/8 NSCLC cell lines that correlated with VEGFR2 mRNA expression levels. VEGF-dependent VEGFR2 activation was apparent in NSCLC cells, and was associated with increased tumor cell proliferation. Cediranib treatment or siRNA against VEGFR2 inhibited VEGF-dependent increases in cell proliferation. Inhibition of VEGFR2 tyrosine kinase activity using cediranib was more effective than inhibition of AKT (MK2206) or MEK (AZD6244) for overcoming VEGFR2-driven cell proliferation. VEGF treatment did not affect cell survival following treatment with radiation, cisplatin, docetaxel or gemcitabine. Our data suggest that a subset of NSCLC tumour cells express functional VEGFR2 which can act to promote VEGF-dependent tumour cell growth. In this tumour subset, therapies targeting VEGFR2 signalling, such as cediranib, have the potential to inhibit both tumour cell proliferation and angiogenesis.

Indexed as

BenzimidazolesCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHeterocyclic Compounds, 3-RingHumansIndolesLung NeoplasmsProtein Kinase InhibitorsQuinazolinesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2AZD 6244BenzimidazolescediranibHeterocyclic Compounds, 3-RingIndolesKDR protein, humanMK 2206Protein Kinase InhibitorsQuinazolinesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID26179332
PMCPMC4532222
OpenAlexW1845735387

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.