Evidence map›Paper›PMID 28463229›Full record

ArticleThe Journal of clinical investigation2017

Comparative oncogenomics identifies tyrosine kinase FES as a tumor suppressor in melanoma.

Michael Olvedy, Julie C Tisserand, Flavie Luciani, Bram Boeckx, Jasper Wouters, Sophie Lopez, Florian Rambow, Sara Aibar, Bernard Thienpont, Jasmine Barra and 9 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. The Roles of PTEN in Melanoma Suppression.Pigment cell & melanoma research · 2025
    Review
  4. Article
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  8. Review
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  13. Article
  14. Epigenetically Silenced Candidate Tumor Suppressor Genes in Prostate Cancer: Identified by Modeling Methylation Stratification and Applied to Progression Prediction.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    Article
  15. Article
  16. The Ashitaba (Cancer prevention research (Philadelphia, Pa.) · 2018
    Article
  17. Article
  18. 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

19 authors at 7 institutions in 4 countries.

Michael OlvedyLaboratory for Molecular Cancer Biology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven, Belgium.
Julie C TisserandINSERM, Aix Marseille University, CNRS, Institut Paoli-Calmettes, CRCM, Equipe Labellisée Ligue Contre le Cancer, Marseille, France.
Flavie LucianiLaboratory for Molecular Cancer Biology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven, Belgium.
Bram BoeckxLaboratory for Translational Genetics, Center for Cancer Biology, VIB, Leuven, Belgium.
Jasper WoutersLaboratory of Computational Biology, Department of Human Genetics, KU Leuven, Leuven, Belgium.
Sophie LopezINSERM, Aix Marseille University, CNRS, Institut Paoli-Calmettes, CRCM, Equipe Labellisée Ligue Contre le Cancer, Marseille, France.
Florian RambowLaboratory for Molecular Cancer Biology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven, Belgium.
Sara AibarLaboratory of Computational Biology, Department of Human Genetics, KU Leuven, Leuven, Belgium.
Bernard ThienpontLaboratory for Translational Genetics, Center for Cancer Biology, VIB, Leuven, Belgium.
Jasmine BarraLaboratory for Molecular Cancer Biology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven, Belgium.
Corinna KöhlerLaboratory for Molecular Cancer Biology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven, Belgium.
Enrico RadaelliMouse Histopathology Core Facility, VIB Center for Brain & Disease Research, Leuven, Belgium.
Sophie Tartare-DeckertCentre Méditerranéen de Médecine Moléculaire (C3M), INSERM, U1065, Université Côte d'Azur, Nice, France.
Stein AertsLaboratory of Computational Biology, Department of Human Genetics, KU Leuven, Leuven, Belgium.
Patrice DubreuilINSERM, Aix Marseille University, CNRS, Institut Paoli-Calmettes, CRCM, Equipe Labellisée Ligue Contre le Cancer, Marseille, France.
Joost J van den OordLaboratory of Translational Cell and Tissue Research, Department of Pathology, KU Leuven and UZ Leuven, Leuven, Belgium.
Diether LambrechtsLaboratory for Translational Genetics, Center for Cancer Biology, VIB, Leuven, Belgium.
Paulo De SepulvedaINSERM, Aix Marseille University, CNRS, Institut Paoli-Calmettes, CRCM, Equipe Labellisée Ligue Contre le Cancer, Marseille, France.
Jean-Christophe MarineLaboratory for Molecular Cancer Biology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven, Belgium.
Vlaams Instituut voor Biotechnologie · BECentre National de la Recherche Scientifique · FRCenter for Human Genetics · USVIB-KU Leuven Center for Cancer Biology · BEInserm · FRUniversitair Ziekenhuis Leuven · BEVIB-KU Leuven Center for Brain & Disease Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identification and functional validation of oncogenic drivers are essential steps toward advancing cancer precision medicine. Here, we have presented a comprehensive analysis of the somatic genomic landscape of the widely used BRAFV600E- and NRASQ61K-driven mouse models of melanoma. By integrating the data with publically available genomic, epigenomic, and transcriptomic information from human clinical samples, we confirmed the importance of several genes and pathways previously implicated in human melanoma, including the tumor-suppressor genes phosphatase and tensin homolog (PTEN), cyclin dependent kinase inhibitor 2A (CDKN2A), LKB1, and others. Importantly, this approach also identified additional putative melanoma drivers with prognostic and therapeutic relevance. Surprisingly, one of these genes encodes the tyrosine kinase FES. Whereas FES is highly expressed in normal human melanocytes, FES expression is strongly decreased in over 30% of human melanomas. This downregulation correlates with poor overall survival. Correspondingly, engineered deletion of Fes accelerated tumor progression in a BRAFV600E-driven mouse model of melanoma. Together, these data implicate FES as a driver of melanoma progression and demonstrate the potential of cross-species oncogenomic approaches combined with mouse modeling to uncover impactful mutations and oncogenic driver alleles with clinical importance in the treatment of human cancer.

Indexed as

AnimalsCell Line, TumorCell ProliferationDNA Copy Number VariationsGenes, Tumor SuppressorGenomicsHumansMelanomaMice, Inbred C57BLMice, NudeMice, TransgenicNeoplasm TransplantationOncogenesProto-Oncogene Proteins c-fesSkin NeoplasmsWnt Signaling PathwayFes protein, mouseProto-Oncogene Proteins c-fes

Identifiers

PMID28463229
PMCPMC5451227
OpenAlexW2611498928

What Socratic 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 Socratic graph.