Evidence map›Paper›PMID 25595897›Full record

ArticleOncotarget2015

Targeting VEGFR1- and VEGFR2-expressing non-tumor cells is essential for esophageal cancer therapy.

Wen Wen Xu, Bin Li, Alfred K Y Lam, Sai Wah Tsao, Simon Y K Law, Kwok Wah Chan, Qiu Ju Yuan, Annie L M Cheung

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 69 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 3 countries.

Wen Wen XuDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Bin LiDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Alfred K Y LamDepartment of Pathology, Griffith Medical School and Griffith Health Institute, Gold Coast Campus, Gold Coast, QLD 4222, Australia.
Sai Wah TsaoDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Simon Y K LawCentre for Cancer Research, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Kwok Wah ChanThe University of Hong Kong-Shenzhen Institute of Research and Innovation (HKU-SIRI), China.
Qiu Ju YuanDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
Annie L M CheungDepartment of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
University of Hong Kong · HKCity University of Hong Kong, Shenzhen Research Institute · CNGriffith University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing appreciation of tumor heterogeneity and the tumor-host interaction has stimulated interest in developing novel therapies that target both tumor cells and tumor microenvironment. Bone marrow derived cells (BMDCs) constitute important components of the tumor microenvironment. In this study, we aim to investigate the significance of VEGFR1- and VEGFR2-expressing non-tumor cells, including BMDCs, in esophageal cancer (EC) progression and in VEGFR1/VEGFR2-targeted therapies. Here we report that VEGFR1 or VEGFR2 blockade can significantly attenuate VEGF-induced Src and Erk signaling, as well as the proliferation and migration of VEGFR1⁺ and VEGFR2⁺ bone marrow cells and their pro-invasive effect on cancer cells. Importantly, our in vivo data show for the first time that systemic blockade of VEGFR1⁺ or VEGFR2⁺ non-tumor cells with neutralizing antibodies is sufficient to significantly suppress esophageal tumor growth, angiogenesis and metastasis in mice. Moreover, our tissue microarray study of human EC clinical specimens showed the clinicopathological significance of VEGFR1 and VEGFR2 in EC, which suggest that anti-VEGFR1/VEGFR2 therapies may be particularly beneficial for patients with aggressive EC. In conclusion, this study demonstrates the important contributions of VEGFR1⁺ and VEGFR2⁺ non-tumor cells in esophageal cancer progression, and substantiates the validity of these receptors as therapeutic targets for this deadly disease.

Indexed as

AnimalsAntibodies, NeutralizingEsophageal NeoplasmsFemaleHumansImmunohistochemistryMaleMiceMice, NudeMolecular Targeted TherapyNeoplasm StagingNeovascularization, PathologicTumor MicroenvironmentVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2Xenograft Model Antitumor AssaysAntibodies, NeutralizingKDR protein, humanVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID25595897
PMCPMC4359332
OpenAlexW1554682485

What OpenQuestion holds

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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.