Evidence map›Paper›PMID 22157681›Full record

ArticleNature medicine2011

EGFR and MET receptor tyrosine kinase-altered microRNA expression induces tumorigenesis and gefitinib resistance in lung cancers.

Michela Garofalo, Giulia Romano, Gianpiero Di Leva, Gerard Nuovo, Young-Jun Jeon, Apollinaire Ngankeu, Jin Sun, Francesca Lovat, Hansjuerg Alder, Gerolama Condorelli and 7 more

RetractedErratum issuedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 210 papers.

0numbers the graph read from it
0cells of the map it votes in
210citing papers in PubMed
15.5field-weighted citation impact, top 1% 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

210 citing papers in PubMed, 365 citations in OpenAlex.

  1. Trial
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  14. Combination of 7-Aging · 2022
    Article
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  17. Article
  18. Review
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  20. Review

150 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 7 institutions in 4 countries.

Michela GarofaloDepartment of Molecular Virology, Immunology and Medical Genetics, Comprehensive Cancer Center, Ohio State University, Columbus, Ohio, USA.
Giulia Romano
Gianpiero Di Leva
Gerard Nuovo
Young-Jun Jeon
Apollinaire Ngankeu
Jin Sun
Francesca Lovat
Hansjuerg Alder
Gerolama Condorelli
Jeffrey A Engelman
Mayumi Ono
Jin Kyung Rho
Luciano Cascione
Stefano Volinia
Kenneth P Nephew
Carlo M Croce
The Ohio State University · USHarvard University · USIndiana University Bloomington · USInstitute for Experimental Endocrinology and Oncology · ITKyushu University · JPSDN Istituto di Ricerca Diagnostica e Nucleare · ITUniversity of Ulsan · KR

Funding

Predicting Drug Resistance in Cancer Genomes by DMA Methylation ProfilingU54CA113001 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HUANG, TIM H.-M. · 2004 to 2014
$16.1M
The Role of Epigenetic Factors in Regulation of Coding and Non-Coding HOX GenesP01CA129242 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2009 to 2013
$4.7M
DNA Methylation and Ovarian CancerR01CA085289 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI NEPHEW, KENNETH P · 2002 to 2012
$2.4M
NCI NIH HHS CA113001NCI NIH HHS P01 CA129242NCI NIH HHS R01 CA085289NCI NIH HHS U54 CA113001
6 · The paper itself

Abstract

The involvement of the MET oncogene in de novo and acquired resistance of non-small cell lung cancers (NSCLCs) to tyrosine kinase inhibitors (TKIs) has previously been reported, but the precise mechanism by which MET overexpression contributes to TKI-resistant NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand their role in TKI-resistant NSCLCs, we examined changes in miRNA that are mediated by tyrosine kinase receptors. Here we report that miR-30b, miR-30c, miR-221 and miR-222 are modulated by both epidermal growth factor (EGF) and MET receptors, whereas miR-103 and miR-203 are controlled only by MET. We showed that these miRNAs have important roles in gefitinib-induced apoptosis and epithelial-mesenchymal transition of NSCLC cells in vitro and in vivo by inhibiting the expression of the genes encoding BCL2-like 11 (BIM), apoptotic peptidase activating factor 1 (APAF-1), protein kinase C ɛ (PKC-ɛ) and sarcoma viral oncogene homolog (SRC). These findings suggest that modulation of specific miRNAs may provide a therapeutic approach for the treatment of NSCLCs.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCell Transformation, NeoplasticDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionErbB ReceptorsGefitinibGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiceAntineoplastic AgentsEGFR protein, humanErbB ReceptorsGefitinibMET protein, humanMicroRNAsProto-Oncogene Proteins c-metQuinazolines

Identifiers

PMID22157681
PMCPMC3467100
OpenAlexW2124808167

What OpenQuestion holds

Textmetadata
LicenceTDM
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.