Evidence map›Paper›PMID 12556241›Full record

ReviewMolecular cancer2003

Pathways for aberrant angiogenesis in pancreatic cancer.

M Korc

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing 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

81 citing papers in PubMed, 171 citations in OpenAlex.

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  10. The Supression of Migration and Metastasis via Inhibition of Vascular Endothelial Growth Factor in Pancreatic Adenocarcinoma Cells Applied Danusertib.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
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21 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

M KorcDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of California, Irvine, California 92697, USA. mkorc@uci.edu
University of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease. Although the specific mechanisms that dictate its biological aggressiveness are not clearly established, it is characterized by a variety of molecular alterations as well as by the overexpression of mitogenic and angiogenic growth factors and their receptors. PDACs also express high levels of vascular endothelial growth factor (VEGF). Recent studies indicate that suppression of VEGF expression attenuates pancreatic cancer cell tumorigenicity in a nude mouse model, and that VEGF can exert direct mitogenic effects on some pancreatic cancer cells. These findings suggest that cancer cell derived VEGF promotes pancreatic cancer growth in vivo via a paracrine angiogenic pathway and an autocrine mitogenic pathway, and provide novel opportunities for therapeutic intervention in this deadly disease.

Indexed as

Signal TransductionAnimalsCarcinoma, Pancreatic DuctalHumansNeovascularization, PathologicPancreatic NeoplasmsReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factor AReceptors, Vascular Endothelial Growth FactorVascular Endothelial Growth Factor A

Identifiers

PMID12556241
PMCPMC149422
OpenAlexW1949135884

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.