Evidence map›Paper›PMID 25807551›Full record

ArticlePloS one2015

Tumor angiogenesis in the absence of fibronectin or its cognate integrin receptors.

Patrick A Murphy, Shahinoor Begum, Richard O Hynes

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 54 citations in OpenAlex.

  1. Testing cellular provenance in the cancer extracellular matrix.Frontiers in cell and developmental biology · 2026
    Review
  2. Article
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  7. Integrin Alpha v Beta 6 (αvβ6) and Its Implications in Cancer Treatment.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Integrin Signaling in Glioma Pathogenesis: From Biology to Therapy.International journal of molecular sciences · 2020
    Review
  13. The Roles of Integrin α5β1 in Human Cancer.OncoTargets and therapy · 2020
    Review
  14. Review
  15. Review
  16. Emerging strategies to disrupt the central TGF-β axis in kidney fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019
    Review
  17. Review
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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

3 authors at 2 institutions in 1 country.

Patrick A MurphyHoward Hughes Medical Institute, David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, United States of America.
Shahinoor BegumHoward Hughes Medical Institute, David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, United States of America.
Richard O HynesHoward Hughes Medical Institute, David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, United States of America.
Massachusetts Institute of Technology · USHoward Hughes Medical Institute · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Platelets in Cardiovascular Biology and PathologyP01HL066105 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KRIEGER, MONTY · 2001 to 2010
$28.4M
Alternative splicing in the vascular response to pathological shear stressF32HL110484 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MURPHY, PATRICK ANDRIES · 2012 to 2014
$156k
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014051NCI NIH HHS P30-CA14051NHLBI NIH HHS 5F32HL110484NHLBI NIH HHS F32 HL110484NHLBI NIH HHS P01 HL066105NHLBI NIH HHS P01-HL66105
6 · The paper itself

Abstract

Binding of α5β1 and αvβ3/β5 integrin receptors on the endothelium to their fibronectin substrate in the extracellular matrix has been targeted as a possible means of blocking tumor angiogenesis and tumor growth. However, clinical trials of blocking antibodies and peptides have been disappointing despite promising preclinical results, leading to questions about the mechanism of the inhibitors and the reasons for their failure. Here, using tissue-specific and inducible genetics to delete the α5 and αv receptors in the endothelium or their fibronectin substrate, either in the endothelium or globally, we show that both are dispensable for tumor growth, in transplanted tumors as well as spontaneous and angiogenesis-dependent RIP-Tag-driven pancreatic adenocarcinomas. In the nearly complete absence of fibronectin, no differences in vascular density or the deposition of basement membrane laminins, ColIV, Nid1, Nid2, or the TGFβ binding matrix proteins, fibrillin-1 and -2, could be observed. Our results reveal that fibronectin and the endothelial fibronectin receptor subunits, α5 and αv, are dispensable for tumor angiogenesis, suggesting that the inhibition of angiogenesis induced by antibodies or small molecules may occur through a dominant negative effect, rather than a simple functional block.

Indexed as

AdenocarcinomaAdipokinesAnimalsBasement MembraneCalcium-Binding ProteinsCell Adhesion MoleculesEndotheliumExtracellular MatrixFibrillin-1FibrillinsFibronectinsIntegrin alpha5beta1IntegrinsMembrane GlycoproteinsMiceMicrofilament ProteinsAdipokinesCalcium-Binding ProteinsCell Adhesion MoleculesFbn1 protein, mouseFibrillin-1FibrillinsFibronectinsIntegrin alpha5beta1IntegrinsMembrane GlycoproteinsMicrofilament ProteinsNid2 protein, mousenidogenTransforming Growth Factor beta

Identifiers

PMID25807551
PMCPMC4373772
OpenAlexW2061599085

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.