Evidence map›Paper›PMID 27033458›Full record

ArticleCancer gene therapy2016

VEGF121 and VEGF165 differentially promote vessel maturation and tumor growth in mice and humans.

M Kazemi, A Carrer, S Moimas, L Zandonà, R Bussani, B Casagranda, S Palmisano, P Prelazzi, M Giacca, L Zentilin and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
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  12. EMID2 is a novel biotherapeutic for aggressive cancers identified by in vivo screening.Journal of experimental & clinical cancer research : CR · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. The VEGF/VEGFR Axis Revisited: Implications for Cancer Therapy.International journal of molecular sciences · 2022
    Review
  18. The emerging era of personalized medicine in advanced colorectal cancer.Journal of gastroenterology and hepatology · 2022
    Review
  19. Article
  20. Review
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

13 authors at 2 institutions in 1 country.

M KazemiMolecular Medicine, International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy.
A CarrerMolecular Medicine, International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy.
S MoimasMolecular Medicine, International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy.
L ZandonàDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
R BussaniDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
B CasagrandaDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
S PalmisanoDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
P PrelazziDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
M GiaccaDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
L ZentilinMolecular Medicine, International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy.
N De ManziniDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
M GiaccaMolecular Medicine, International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy.
S ZacchignaDepartment of Medical, Surgical and Health Sciences, University Hospital of Trieste, Trieste, Italy.
University of Trieste · ITInternational Centre for Genetic Engineering and Biotechnology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor angiogenesis depends on the vascular endothelial growth factor (VEGF), which exists in multiple splicing isoforms, including the most abundant VEGF165 and VEGF121. We have previously shown that the differential capacity of these two VEGF isoforms to bind Neuropilin-1 accounts for their diverse ability to recruit Nrp1-expressing monocytes (NEMs), resulting in a different arteriogenic potential. Here we measure the expression of VEGF165 and VEGF121 in human cancer and their influence on tumor growth and vascularization. We measured the expression levels of VEGF165 and VEGF121 in human colorectal cancer and found that VEGF121 was more expressed than VEGF165, particularly in patients with extensive lymph node infiltration. Overexpressing either VEGF165 or VEGF121 in a cancer mouse model, we observed that the former decreased, whereas the latter increased tumor growth. In both clinical and experimental tumors, VEGF165 expression resulted in the recruitment of NEMs, paralleled by maturation of the tumor vascular network. Finally, hypoxia induced a shift toward the VEGF165 isoform in the central core of human cancers, as well as in various types of cultured cells. These results demonstrate that the two VEGF splicing isoforms are differentially expressed in colorectal cancers, exerting opposite effects on tumor growth and vessel maturation.

Indexed as

Gene Expression Regulation, NeoplasticAlternative SplicingAnimalsCell Line, TumorDependovirusDisease Models, AnimalGenetic VectorsHumansHypoxiaImmunohistochemistryLymphatic MetastasisMelanoma, ExperimentalMiceNeoplasmsNeovascularization, PathologicProtein IsoformsProtein IsoformsVascular Endothelial Growth Factor A

Identifiers

PMID27033458
OpenAlexW2316373260

What OpenQuestion holds

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Registered trials

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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.