Evidence map›Paper›PMID 38791979›Full record

ArticleCancers2024

An Anti-VEGF-B Antibody Reduces Abnormal Tumor Vasculature and Enhances the Effects of Chemotherapy.

Peter W Janes, Adam C Parslow, Diana Cao, Angela Rigopoulos, Fook-Thean Lee, Sylvia J Gong, Glenn A Cartwright, Ingrid J G Burvenich, Ulf Eriksson, Terrance G Johns and 2 more

Abstract read
In one paragraph

Article in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. 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

12 authors.

Peter W JanesTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.ORCID 0000-0002-9039-1097
Adam C ParslowTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.ORCID 0000-0002-9868-6914
Diana CaoTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.
Angela RigopoulosTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.
Fook-Thean LeeTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.
Sylvia J GongSchool of Computing, Engineering and Mathematical Sciences, La Trobe University, Melbourne, VIC 3083, Australia.
Glenn A CartwrightTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.ORCID 0009-0006-6008-6354
Ingrid J G BurvenichTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.ORCID 0000-0001-8384-2403
Ulf ErikssonDivision of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institute, 171 77 Solna, Sweden.
Terrance G JohnsOncogenic Signalling Laboratory, Telethon Kids Cancer Centre, Telethon Kids Institute, Nedlands, WA 6009, Australia.ORCID 0000-0002-8874-4543
Fiona E ScottTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.
Andrew M ScottTumour Targeting Program, Olivia Newton-John Cancer Research Institute, Heidelberg, VIC 3084, Australia.

Funding

CSL Ltd Not applicableNational Health and Medical Research Council 1177837Swedish Research Council 2017-01794
6 · The paper itself

Abstract

The vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are key regulators of blood vessel formation, including in tumors, where their deregulated function can promote the production of aberrant, leaky blood vessels, supporting tumor development. Here we investigated the VEGFR1 ligand VEGF-B, which we demonstrate to be expressed in tumor cells and in tumor stroma and vasculature across a range of tumor types. We examined the anti-VEGF-B-specific monoclonal antibody 2H10 in preclinical xenograft models of breast and colorectal cancer, in comparison with the anti-VEGF-A antibody bevacizumab. Similar to bevacizumab, 2H10 therapy was associated with changes in tumor blood vessels and intra-tumoral diffusion consistent with normalization of the tumor vasculature. Accordingly, treatment resulted in partial inhibition of tumor growth, and significantly improved the response to chemotherapy. Our studies indicate the importance of VEGF-B in tumor growth, and the potential of specific anti-VEGF-B treatment to inhibit tumor development, alone or in combination with established chemotherapies.

Indexed as

antibodytherapeutictumor angiogenesisvessel normalization

Identifiers

PMID38791979
PMCPMC11119922

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.