Evidence map›Paper›PMID 42477455›Full record

ArticleEMBO molecular medicine2026

Selective mRNA translation determines adaptative mutability of melanoma cells to anti-BRAF/MEK combination therapy.

Lucilla Fabbri, Lucie Lagadec, Eva Guérin, Hélène Lecourt, Dorothée Baille, Laetitia Besse, Cédric Messaoudi, Laurent Désaubry, Hussein Abou-Hamdan, Sévérine Roy and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Article
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

15 authors.

Lucilla FabbriInstitut Curie, PSL Research University, CNRS UMR3348, INSERM U1368, Orsay, France. lucilla.fabbri@curie.fr.ORCID http://orcid.org/0000-0003-2928-3983
Lucie LagadecInstitut Curie, PSL Research University, CNRS UMR3348, INSERM U1368, Orsay, France.
Eva GuérinInstitut Curie, PSL Research University, CNRS UMR3348, INSERM U1368, Orsay, France.ORCID http://orcid.org/0000-0003-0549-4946
Hélène LecourtINSERM U981, Gustave Roussy Cancer Campus, Villejuif, France.
Dorothée BailleInstitut Curie, PSL Research University, CNRS UMR3348, INSERM U1368, Orsay, France.ORCID http://orcid.org/0000-0001-7257-8408
Laetitia BesseInstitut Curie, PSL University, CNRS UAR2016, Inserm US43, Université Paris-Saclay, Multimodal Imaging Center, Orsay, France.
Cédric MessaoudiInstitut Curie, PSL University, CNRS UAR2016, Inserm US43, Université Paris-Saclay, Multimodal Imaging Center, Orsay, France.ORCID http://orcid.org/0000-0003-3535-7723
Laurent DésaubryCenter of Research in Biomedicine of Strasbourg, Regenerative Nanomedicine (UMR 1260), INSERM, University of Strasbourg, Strasbourg, France.
Hussein Abou-HamdanCenter of Research in Biomedicine of Strasbourg, Regenerative Nanomedicine (UMR 1260), INSERM, University of Strasbourg, Strasbourg, France.
Sévérine RoyINSERM U981, Gustave Roussy Cancer Campus, Villejuif, France.
Bérangère LombardInstitut Curie, PSL University, CurieCoreTech Mass Spectrometry Proteomics, Paris, France.
Damarys LoewInstitut Curie, PSL University, CurieCoreTech Mass Spectrometry Proteomics, Paris, France.ORCID http://orcid.org/0000-0002-9111-8842
Jean-Yves ScoazecInstitut Gustave Roussy, INSERM U1015, Bâtiment de Médecine Moléculaire 114 rue Edouard Vaillant, 94800, Villejuif, France.ORCID http://orcid.org/0000-0003-1604-6823
Caroline RobertINSERM U981, Gustave Roussy Cancer Campus, Villejuif, France.ORCID http://orcid.org/0000-0002-9493-0238
Stéphan VagnerInstitut Curie, PSL Research University, CNRS UMR3348, INSERM U1368, Orsay, France. stephan.vagner@curie.fr.ORCID http://orcid.org/0000-0003-1452-7164

Funding

INSERM 21CQ016-00Région Ile de France NEX061034SIRIC Curie / INCa-DGOS-Inserm-ITMO Cancer 18000
6 · The paper itself

Abstract

During their inevitable evolution towards acquired resistance to anti-cancer targeted therapies, cancer cells adopt distinct gene expression profiles that allow them to transiently adapt to and tolerate the treatment. Cancer cells surviving therapy can increase their mutation rate, enhancing the likelihood of acquiring resistance-conferring mutations and evolving into resistant cells. Here we show that translational control mediates the adaptive mutability of melanoma drug-tolerant cells by regulating the translation of the error-prone non-homologous end joining (NHEJ) component 53BP1. The specific inhibition of 5'UTR-driven 53BP1 mRNA translation was sufficient to impair NHEJ and mutability. We found that the eIF4A RNA helicase, regulates 53BP1 mRNA translation. Consequently, targeting the eIF4A with two small molecule inhibitors significantly delays the acquisition of resistance to combination of BRAF and MEK inhibitors in BRAF

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmMelanomaProtein BiosynthesisProtein Kinase InhibitorsProto-Oncogene Proteins B-rafRNA, MessengerAnimalsCell Line, TumorEukaryotic Initiation Factor-4AHumansMiceMutationAntineoplastic AgentsBRAF protein, humanEukaryotic Initiation Factor-4AProtein Kinase InhibitorsProto-Oncogene Proteins B-rafRNA, Messenger

Identifiers

PMID42477455
PMCPMC13470486

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.