Evidence map›Paper›PMID 25157817›Full record

ArticleThe Journal of clinical investigation2014

Endothelial deficiency of L1 reduces tumor angiogenesis and promotes vessel normalization.

Elena Magrini, Alessandra Villa, Francesca Angiolini, Andrea Doni, Giovanni Mazzarol, Noemi Rudini, Luigi Maddaluno, Mina Komuta, Baki Topal, Hans Prenen and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  14. L1CAM promotes ovarian cancer stemness and tumor initiation via FGFR1/SRC/STAT3 signaling.Journal of experimental & clinical cancer research : CR · 2021
    Article
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  18. Review
  19. Review
  20. L1CAM as an E-selectin Ligand in Colon Cancer.International journal of molecular sciences · 2020
    Article
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

16 authors at 5 institutions in 3 countries.

Elena Magrini
Alessandra Villa
Francesca Angiolini
Andrea Doni
Giovanni Mazzarol
Noemi Rudini
Luigi Maddaluno
Mina Komuta
Baki Topal
Hans Prenen
Melitta Schachner
Stefano Confalonieri
Elisabetta Dejana
Fabrizio Bianchi
Massimiliano Mazzone
Ugo Cavallaro
European Institute of Oncology · ITKU Leuven · BEFIRC Institute of Molecular Oncology · ITFondazione Humanitas per la Ricerca · ITRutgers, The State University of New Jersey · US

Funding

Telethon GGP04078Worldwide Cancer Research 10-0091
6 · The paper itself

Abstract

While tumor blood vessels share many characteristics with normal vasculature, they also exhibit morphological and functional aberrancies. For example, the neural adhesion molecule L1, which mediates neurite outgrowth, fasciculation, and pathfinding, is expressed on tumor vasculature. Here, using an orthotopic mouse model of pancreatic carcinoma, we evaluated L1 functionality in cancer vessels. Tumor-bearing mice specifically lacking L1 in endothelial cells or treated with anti-L1 antibodies exhibited decreased angiogenesis and improved vascular stabilization, leading to reduced tumor growth and metastasis. In line with these dramatic effects of L1 on tumor vasculature, the ectopic expression of L1 in cultured endothelial cells (ECs) promoted phenotypical and functional alterations, including proliferation, migration, tubulogenesis, enhanced vascular permeability, and endothelial-to-mesenchymal transition. L1 induced global changes in the EC transcriptome, altering several regulatory networks that underlie endothelial pathophysiology, including JAK/STAT-mediated pathways. In particular, L1 induced IL-6-mediated STAT3 phosphorylation, and inhibition of the IL-6/JAK/STAT signaling axis prevented L1-induced EC proliferation and migration. Evaluation of patient samples revealed that, compared with that in noncancerous tissue, L1 expression is specifically enhanced in blood vessels of human pancreatic carcinomas and in vessels of other tumor types. Together, these data indicate that endothelial L1 orchestrates multiple cancer vessel functions and represents a potential target for tumor vascular-specific therapies.

Indexed as

Neovascularization, PathologicAnimalsBlood VesselsCapillary PermeabilityCarcinomaCell MovementCell ProliferationEndothelial CellsEndothelium, VascularFemaleHemangiomaHumansInterleukin-6MaleMiceMice, Inbred C57BLInterleukin-6Neural Cell Adhesion Molecule L1Receptor, TIE-2Stat3 protein, mouseSTAT3 Transcription FactorTek protein, mouse

Identifiers

PMID25157817
PMCPMC4191010
OpenAlexW2034126562

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.