Evidence map›Paper›PMID 28003335›Full record

ArticleEMBO molecular medicine2017

The RAS-related GTPase RHOB confers resistance to EGFR-tyrosine kinase inhibitors in non-small-cell lung cancer via an AKT-dependent mechanism.

Olivier Calvayrac, Julien Mazières, Sarah Figarol, Claire Marty-Detraves, Isabelle Raymond-Letron, Emilie Bousquet, Magali Farella, Estelle Clermont-Taranchon, Julie Milia, Isabelle Rouquette and 7 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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

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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

17 authors at 7 institutions in 1 country.

Olivier CalvayracInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France.
Julien MazièresInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France mazieres.j@chu-toulouse.fr favre.gilles@iuct-oncopole.fr.ORCID 0000-0002-5921-7613
Sarah FigarolInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France.
Claire Marty-DetravesInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France.
Isabelle Raymond-LetronLaboratoire d'Histopathologie, UPS-INP-ENVT, UMS006, Université de Toulouse, Toulouse, France.
Emilie BousquetCHU Toulouse, IUCT-Rangueil-Larrey, Service de Pneumologie, Toulouse, France.
Magali FarellaInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France.
Estelle Clermont-TaranchonDepartement d'Anatomo-Cytopathologie, CHU de Toulouse, IUCT-Oncopole, Toulouse, France.
Julie MiliaUniversité Paul Sabatier, Toulouse, France.
Isabelle RouquetteDepartement d'Anatomo-Cytopathologie, CHU de Toulouse, IUCT-Oncopole, Toulouse, France.
Nicolas GuibertInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France.
Amélie LusqueInstitut Claudius Regaud, IUCT-Oncopole, Bureau des Essais Cliniques, Cellule Biostatistiques, Toulouse, France.
Jacques CadranelSorbonne Universités UPMC Univ. Paris 06 GRC n°04 Theranoscan, Paris AP-HP, Hôpital Tenon, Service de Pneumologie, Paris, France.
Nathalie MathiotSorbonne Universités UPMC Univ. Paris 06 GRC n°04 Theranoscan, Paris AP-HP, Hôpital Tenon, Service de Pneumologie, Paris, France.
Ariel SavinaInstitut Roche, Roche SAS, Boulogne-Billancourt, France.
Anne PradinesInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France.
Gilles FavreInserm, Centre de Recherche en Cancérologie de Toulouse, CRCT UMR-1037, Toulouse, France mazieres.j@chu-toulouse.fr favre.gilles@iuct-oncopole.fr.ORCID 0000-0002-2344-1883
Inserm · FRUniversité Toulouse III - Paul Sabatier · FRCentre Hospitalier Universitaire de Toulouse · FRSorbonne Université · FRHôpital Larrey · FRInstitut Claudius Regaud · FRRoche (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although lung cancer patients harboring EGFR mutations benefit from treatment with EGFR-tyrosine kinase inhibitors (EGFR-TKI), most of them rapidly relapse. RHOB GTPase is a critical player in both lung carcinogenesis and the EGFR signaling pathway; therefore, we hypothesized that it could play a role in the response to EGFR-TKI In a series of samples from EGFR-mutated patients, we found that low RHOB expression correlated with a good response to EGFR-TKI treatment while a poor response correlated with high RHOB expression (15.3 versus 5.6 months of progression-free survival). Moreover, a better response to EGFR-TKI was associated with low RHOB levels in a panel of lung tumor cell lines and in a lung-specific tetracycline-inducible EGFR

Indexed as

Drug ResistanceAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungEnzyme InhibitorsErbB ReceptorsHumansMiceMice, TransgenicProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktrhoB GTP-Binding ProteinAntineoplastic AgentsEGFR protein, humanEnzyme InhibitorsErbB ReceptorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktrhoB GTP-Binding ProteinAKTEGFRresistanceRhoBTKI

Identifiers

PMID28003335
PMCPMC5286377
OpenAlexW2563456733

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.