Evidence map›Paper›PMID 10751370›Full record

ArticleThe American journal of pathology2000

Overexpression of VEGF 121 in immortalized endothelial cells causes conversion to slowly growing angiosarcoma and high level expression of the VEGF receptors VEGFR-1 and VEGFR-2 in vivo.

J L Arbiser, H Larsson, L Claesson-Welsh, X Bai, K LaMontagne, S W Weiss, S Soker, E Flynn, L F Brown

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-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

25 citing papers in PubMed, 119 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

9 authors at 4 institutions in 2 countries.

J L ArbiserDepartment of Dermatology, Emory University School of Medicine, Atlanta, Georgia 30322, USA. jarbise@emory.edu
H Larsson
L Claesson-Welsh
X Bai
K LaMontagne
S W Weiss
S Soker
E Flynn
L F Brown
Emory University · USHarvard University · USUppsala University · SEBeth Israel Deaconess Medical Center · US

Funding

UV light and the cutaneous neurosensory systemP30AR042687 · NIAMS · EMORY UNIVERSITY · PI CAUGHMAN, STEWART W · 1994 to 2003
$2.5M
PATHOPHYSIOLOGY OF CUTANEOUS VASCULAR LESIONSK08AR002096 · NIAMS · EMORY UNIVERSITY · PI ARBISER, JACK L · 1998 to 2002
$297k
ANGIOGENESIS IN CUTANEOUS VASCULAR TUMORSR03AR044947 · NIAMS · EMORY UNIVERSITY · PI ARBISER, JACK L · 1997 to 1999
–
NIAMS NIH HHS KO8 AR02096-01NIAMS NIH HHS P30 AR042687NIAMS NIH HHS P30 AR 42687NIAMS NIH HHS R03 AR44947-03
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF or vascular permeability factor) is an important angiogenic factor that is up-regulated in numerous benign and malignant disorders, including angiosarcoma, hemangiomas, and solid tumors. To determine the functional role of VEGF in the development of endothelial tumors, we expressed primate VEGF 121 in an endothelial cell line, MS1, derived from primary murine cells by immortalization with a temperature-sensitive SV40 large T antigen. This cell line expresses the VEGFR-2 (Flk-1/Kdr) receptor for VEGF. Expression of VEGF 121 led to the development of slowly growing endothelial tumors, which were histologically well-differentiated angiosarcomas. The angiosarcomas generated from MS1 VEGF cells demonstrated up-regulation of the VEGF receptors VEGFR-2 and VEGFR-1 (Flt-1) in vivo compared with benign hemangiomas generated from MS1 cells. Treatment of these cells with the VEGFR-2 tyrosine kinase inhibitor SU 1498 led to decreased expression of ets-1, a transcription factor which has been shown to be stimulated by VEGF. These results suggest that high level expression of VEGF in endothelial cells may result in malignant transformation. This transformation process likely involves both autocrine and paracrine pathways.

Indexed as

Cell Transformation, NeoplasticAnimalsCell Line, TransformedEndothelial Growth FactorsEndothelium, VascularEnzyme InhibitorsHemangiosarcomaLymphokinesMaleMiceMice, NudePhosphorylationPrimatesProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Growth FactorEndothelial Growth FactorsEnzyme InhibitorsLymphokinesProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth FactorsVEGFA protein, human

Identifiers

PMID10751370
PMCPMC1876889
OpenAlexW2026144900

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.