Evidence map›Paper›PMID 25185646›Full record

ReviewTargeted oncology2015

Angiogenesis and tumor microenvironment: bevacizumab in the breast cancer model.

Olivier Trédan, Magali Lacroix-Triki, Séverine Guiu, Marie-Ange Mouret-Reynier, Jérôme Barrière, François-Clément Bidard, Antoine-Laurent Braccini, Olivier Mir, Christian Villanueva, Philippe Barthélémy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Targeted oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
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  7. Adipocyte and lipid metabolism in cancer drug resistance.The Journal of clinical investigation · 2019
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  19. Establishment of anTechnology in cancer research & treatment
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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

10 authors at 10 institutions in 1 country.

Olivier TrédanDepartment of Medical Oncology, Centre Léon Bérard, 28 rue Laennec, 69373, Lyon Cedex, France, olivier.tredan@lyon.unicancer.fr.
Magali Lacroix-Triki
Séverine Guiu
Marie-Ange Mouret-Reynier
Jérôme Barrière
François-Clément Bidard
Antoine-Laurent Braccini
Olivier Mir
Christian Villanueva
Philippe Barthélémy
Biotherapy of Genetic Diseases, Inflammatory Disorders and Cancers · FRCEA Valduc · FRCentre Antoine Lacassagne · FRCentre Georges François Leclerc · FRCentre Hospitalier Universitaire de Besançon · FRCentre Léon Bérard · FRHôpital Cochin · FRInstitut Claudius Regaud · FRInstitut Curie · FRUniversité Clermont Auvergne · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Solid tumors require blood vessels for growth, and many new cancer therapies are directed against the tumor vasculature. Antiangiogenic therapies should destroy the tumor vasculature, thereby depriving the tumor of oxygen and nutrients. According to Jain et al., an alternative hypothesis could be that certain antiangiogenic agents can also transiently "normalize" the abnormal structure and function of tumor vasculature to make it more efficient for oxygen and drug delivery. With emphasize on the research works of Jain et al., the aim of this review is to describe the impact of antivascular endothelial growth factor (VEGF) therapy on "pseudo-normalization" of tumor vasculature and tumor microenvironment, its role in early and metastatic breast cancer, and the clinical evidence supporting this original concept. The phase III clinical trials showed that extended tumors, metastatic or locally advanced, are likely to benefit from bevacizumab therapy in combination with chemotherapy, assuming that a high level of tumor neoangiogenesis as in triple-negative tumors is the best target. In adjuvant setting, the lower level of tumor vasculature could mask a potential benefit of anti-VEGF therapy. All these findings highlight the need to identify biomarkers to help in the selection of patients most likely to respond to anti-VEGF therapy, to better understand the mechanism of angiogenesis and of resistance to anti-VEGF therapy according to molecular subtypes.

Indexed as

Neovascularization, PathologicTumor MicroenvironmentAngiogenesis InhibitorsAnimalsBevacizumabBiomarkers, TumorBreast NeoplasmsDrug Resistance, NeoplasmFemaleHumansPatient SelectionPredictive Value of TestsSignal TransductionVascular Endothelial Growth Factor AAngiogenesis InhibitorsBevacizumabBiomarkers, TumorVascular Endothelial Growth Factor A

Identifiers

PMID25185646
OpenAlexW2072607744

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.