Evidence map›Paper›PMID 27974353›Full record

ArticleEMBO molecular medicine2017

VEGF blockade enhances the antitumor effect of BRAFV600E inhibition.

Valentina Comunanza, Davide Corà, Francesca Orso, Francesca Maria Consonni, Emanuele Middonti, Federica Di Nicolantonio, Anton Buzdin, Antonio Sica, Enzo Medico, Dario Sangiolo and 2 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2017. 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
1.9field-weighted citation impact, top 12% 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, 39 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Sustained release hydrogel for durable locoregional chemoimmunotherapy for BRAF-mutated melanoma.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Article
  6. Chemical Factory-Guaranteed Enhanced Chemodynamic Therapy for Orthotopic Liver Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  7. Article
  8. Differential association of CD68British journal of cancer · 2020
    Article
  9. Article
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  11. Review
  12. Article
  13. Article
  14. 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

12 authors at 5 institutions in 2 countries.

Valentina ComunanzaDepartment of Oncology, University of Torino, Candiolo, Italy.
Davide CoràDepartment of Oncology, University of Torino, Candiolo, Italy.
Francesca OrsoCenter for Molecular Systems Biology, University of Torino, Orbassano, Italy.
Francesca Maria ConsonniHumanitas Clinical and Research Center, Rozzano, Italy.
Emanuele MiddontiDepartment of Oncology, University of Torino, Candiolo, Italy.
Federica Di NicolantonioDepartment of Oncology, University of Torino, Candiolo, Italy.ORCID 0000-0001-9618-2010
Anton BuzdinLaboratory of Bioinformatics, D. Rogachyov Federal Research Center of Pediatric Hematology, Oncology and Immunology, Moscow, Russia.
Antonio SicaHumanitas Clinical and Research Center, Rozzano, Italy.
Enzo MedicoDepartment of Oncology, University of Torino, Candiolo, Italy.ORCID 0000-0002-3917-2438
Dario SangioloDepartment of Oncology, University of Torino, Candiolo, Italy.
Daniela TavernaCenter for Molecular Systems Biology, University of Torino, Orbassano, Italy.
Federico BussolinoDepartment of Oncology, University of Torino, Candiolo, Italy federico.bussolino@unito.it.
Candiolo Cancer Institute · ITUniversity of Turin · ITHumanitas University · ITKurchatov Institute · RUUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of resistance remains a major obstacle to long-term disease control in cancer patients treated with targeted therapies. In BRAF-mutant mouse models, we demonstrate that although targeted inhibition of either BRAF or VEGF initially suppresses the growth of BRAF-mutant tumors, combined inhibition of both pathways results in apoptosis, long-lasting tumor responses, reduction in lung colonization, and delayed onset of acquired resistance to the BRAF inhibitor PLX4720. As well as inducing tumor vascular normalization and ameliorating hypoxia, this approach induces remodeling of the extracellular matrix, infiltration of macrophages with an M1-like phenotype, and reduction in cancer-associated fibroblasts. At the molecular level, this therapeutic regimen results in a de novo transcriptional signature, which sustains and explains the observed efficacy with regard to cancer progression. Collectively, our findings offer new biological rationales for the management of clinical resistance to BRAF inhibitors based on the combination between BRAF

Indexed as

AnimalsAntineoplastic AgentsDisease Models, AnimalIndolesMiceMutant ProteinsMutation, MissenseNeoplasmsProto-Oncogene Proteins B-rafSulfonamidesTreatment OutcomeVascular Endothelial Growth Factor AAntineoplastic AgentsBraf protein, mouseIndolesMutant ProteinsPLX 4720Proto-Oncogene Proteins B-rafSulfonamidesVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseangiogenesisdrug resistanceextracellular matrixmyeloid infiltrationvascular normalization

Identifiers

PMID27974353
PMCPMC5286370
OpenAlexW2561024845

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.