Evidence map›Paper›PMID 26456302›Full record

ArticleNature communications2015

MAP3K8/TPL-2/COT is a potential predictive marker for MEK inhibitor treatment in high-grade serous ovarian carcinomas.

Tina Gruosso, Camille Garnier, Sophie Abelanet, Yann Kieffer, Vincent Lemesre, Dorine Bellanger, Ivan Bieche, Elisabetta Marangoni, Xavier Sastre-Garau, Virginie Mieulet and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed, 55 citations in OpenAlex.

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  9. Epigenetic Regulation of MAP3K8 in EBV-Associated Gastric Carcinoma.International journal of molecular sciences · 2023
    Article
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  18. Melanocytic tumors with MAP3K8 fusions: report of 33 cases with morphological-genetic correlations.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
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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

11 authors at 2 institutions in 1 country.

Tina GruossoStress and Cancer Laboratory, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Camille GarnierStress and Cancer Laboratory, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Sophie AbelanetStress and Cancer Laboratory, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Yann KiefferStress and Cancer Laboratory, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Vincent LemesreStress and Cancer Laboratory, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Dorine BellangerInserm, Genetics and Biology of Cancers, U830, Paris F-75248, France.
Ivan BiecheDepartment of Pharmacogenomics, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Elisabetta MarangoniTranslational Research Department, Laboratory of Precinical Investigation, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Xavier Sastre-GarauDepartment of Pathology, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Virginie MieuletStress and Cancer Laboratory, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Fatima Mechta-GrigoriouStress and Cancer Laboratory, Institut Curie, 26, rue d'Ulm, Paris 75248, France.
Institut Curie · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is a silent disease with a poor prognosis that urgently requires new therapeutic strategies. In low-grade ovarian tumours, mutations in the MAP3K BRAF gene constitutively activate the downstream kinase MEK. Here we demonstrate that an additional MAP3K, MAP3K8 (TPL-2/COT), accumulates in high-grade serous ovarian carcinomas (HGSCs) and is a potential prognostic marker for these tumours. By combining analyses on HGSC patient cohorts, ovarian cancer cells and patient-derived xenografts, we demonstrate that MAP3K8 controls cancer cell proliferation and migration by regulating key players in G1/S transition and adhesion dynamics. In addition, we show that the MEK pathway is the main pathway involved in mediating MAP3K8 function, and that MAP3K8 exhibits a reliable predictive value for the effectiveness of MEK inhibitor treatment. Our data highlight key roles for MAP3K8 in HGSC and indicate that MEK inhibitors could be a useful treatment strategy, in combination with conventional chemotherapy, for this disease.

Indexed as

AnimalsAntineoplastic AgentsBenzimidazolesBiomarkers, TumorCarcinogenesisCell Line, TumorCystadenocarcinoma, SerousFemaleHumansMAP Kinase Kinase KinasesMAP Kinase Signaling SystemMiceMice, NudeMitogen-Activated Protein Kinase KinasesOvarian NeoplasmsPrognosisAntineoplastic AgentsAZD 6244BenzimidazolesbinimetinibBiomarkers, TumorMAP3K8 protein, humanMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase KinasesProto-Oncogene ProteinsRibosomal Protein S6 Kinases, 90-kDa

Identifiers

PMID26456302
PMCPMC4633961
OpenAlexW2286136774

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Registered trials

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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.