Evidence map›Paper›PMID 15245600›Full record

ArticleCancer science2004

Direct inhibition of EGF receptor activation in vascular endothelial cells by gefitinib ('Iressa', ZD1839).

Akira Hirata, Hisanori Uehara, Keisuke Izumi, Seiji Naito, Michihiko Kuwano, Mayumi Ono

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 43 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

6 authors at 3 institutions in 1 country.

Akira HirataDepartment of Medical Biochemistry, Graduate School of Medical Science, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan.
Hisanori Uehara
Keisuke Izumi
Seiji Naito
Michihiko Kuwano
Mayumi Ono
Kyushu University · JPTokushima University · JPKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of gefitinib ('Iressa', ZD1839) by targeting the EGFR tyrosine kinase is a recent therapeutic highlight. We have reported that gefitinib is antiangiogenic in vitro, as well as in vivo. In this study, we asked if the anti-angiogenic action of gefitinib is due to a direct effect on activation of vascular endothelial cells by EGF. EGF, as well as VEGF, caused pronounced angiogenesis in an avascular area of the mouse cornea, and i.p. administration of gefitinib almost completely blocked the response to EGF, but not to VEGF. Immunohistochemical analysis demonstrated phosphorylation of EGFR by EGF in the neovasculature, and gefitinib markedly reduced this effect. Gefitinib also inhibited downstream activation of ERK 1/2 via EGFR in cultured microvascular endothelial (HMVE) cells. These findings suggest that the anti-angiogenic effect of gefitinib in the vascular endothelial cells of neo-vasculature is partly attributable to direct inhibition of EGFR activation, and that endothelial cells in malignant tumors play a critical role in the cancer therapeutic efficacy of gefitinib.

Indexed as

Neovascularization, PathologicAntineoplastic AgentsBlotting, WesternCell Culture TechniquesEndothelial CellsEpidermal Growth FactorErbB ReceptorsGefitinibHumansImmunohistochemistryProtein-Tyrosine KinasesQuinazolinesAntineoplastic AgentsEpidermal Growth FactorErbB ReceptorsGefitinibProtein-Tyrosine KinasesQuinazolines

Identifiers

PMID15245600
PMCPMC11159076
OpenAlexW2098765174

What OpenQuestion holds

Textmetadata
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.