Evidence map›Paper›PMID 28497782›Full record

ArticleNature communications2017

RAF proteins exert both specific and compensatory functions during tumour progression of NRAS-driven melanoma.

Coralie Dorard, Charlène Estrada, Céline Barbotin, Magalie Larcher, Alexandra Garancher, Jessy Leloup, Friedrich Beermann, Manuela Baccarini, Celio Pouponnot, Lionel Larue and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-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

34 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Identification ofInternational journal of molecular sciences · 2022
    Article
  12. Review
  13. A Series of BRAF- and NRAS-Driven Murine Melanoma Cell Lines with Inducible Gene Modulation Capabilities.JID innovations : skin science from molecules to population health · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Classification and Grading of Melanocytic Lesions in a Mouse Model ofThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Article
  20. Current Perspectives and Novel Strategies ofOncoTargets and therapy · 2021
    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 at 3 institutions in 3 countries.

Coralie DorardInstitut Curie, Orsay F-91405, France.
Charlène EstradaInstitut Curie, Orsay F-91405, France.
Céline BarbotinInstitut Curie, Orsay F-91405, France.
Magalie LarcherInstitut Curie, Orsay F-91405, France.
Alexandra GarancherInstitut Curie, Orsay F-91405, France.
Jessy LeloupInstitut Curie, Orsay F-91405, France.
Friedrich BeermannSwiss Institute for Experimental Cancer Research (ISREC), Ecole Polytechnique Fédérale de Lausanne, Lausanne 1015, Switzerland.
Manuela BaccariniMax F. Perutz Laboratories, Center for Molecular Biology, University of Vienna, Vienna 1030, Austria.ORCID 0000-0002-3033-391X
Celio PouponnotInstitut Curie, Orsay F-91405, France.
Lionel LarueInstitut Curie, Orsay F-91405, France.
Alain EychèneInstitut Curie, Orsay F-91405, France.
Sabine DruillennecInstitut Curie, Orsay F-91405, France.
Université Paris-Sud · FRÉcole Polytechnique Fédérale de Lausanne · CHUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NRAS and its effector BRAF are frequently mutated in melanoma. Paradoxically, CRAF but not BRAF was shown to be critical for various RAS-driven cancers, raising the question of the role of RAF proteins in NRAS-induced melanoma. Here, using conditional ablation of Raf genes in NRAS-induced mouse melanoma models, we investigate their contribution in tumour progression, from the onset of benign tumours to malignant tumour maintenance. We show that BRAF expression is required for ERK activation and nevi development, demonstrating a critical role in the early stages of NRAS-driven melanoma. After melanoma formation, single Braf or Craf ablation is not sufficient to block tumour growth, showing redundant functions for RAF kinases. Finally, proliferation of resistant cells emerging in the absence of BRAF and CRAF remains dependent on ARAF-mediated ERK activation. These results reveal specific and compensatory functions for BRAF and CRAF and highlight an addiction to RAF signalling in NRAS-driven melanoma.

Indexed as

AnimalsCell Line, TumorDisease ProgressionHumansMAP Kinase Signaling SystemMelanomaMice, Inbred C57BLMice, KnockoutMice, TransgenicMonomeric GTP-Binding ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafras ProteinsMonomeric GTP-Binding ProteinsNras protein, mouseProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafras Proteins

Identifiers

PMID28497782
PMCPMC5437303
OpenAlexW2613470058

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.