Evidence map›Paper›PMID 25784483›Full record

ArticleOncotarget2015

Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer.

Carolina Beatriz Müller, Marco Antônio De Bastiani, Matheus Becker, Fernanda Stapenhorst França, Mariane Araujo Branco, Mauro Antônio Alves Castro, Fabio Klamt

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-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

11 citing papers in PubMed, 21 citations in OpenAlex.

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  10. Expression of Cofilin-1 and Transgelin in Esophageal Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2015
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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

7 authors at 2 institutions in 1 country.

Carolina Beatriz MüllerLaboratory of Cellular Biochemistry, Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre (RS), Brazil.
Marco Antônio De BastianiLaboratory of Cellular Biochemistry, Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre (RS), Brazil.
Matheus BeckerLaboratory of Cellular Biochemistry, Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre (RS), Brazil.
Fernanda Stapenhorst FrançaLaboratory of Cellular Biochemistry, Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre (RS), Brazil.
Mariane Araujo BrancoLaboratory of Cellular Biochemistry, Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre (RS), Brazil.
Mauro Antônio Alves CastroPrograma de Pós-Graduação em Bioinformática, Federal University of Paraná (UFPR), Curitiba (PR), Brazil.
Fabio KlamtLaboratory of Cellular Biochemistry, Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre (RS), Brazil.
Universidade Federal do Rio Grande do Sul · BRUniversidade Federal do Paraná · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current challenge in oncology is to establish the concept of personalized medicine in clinical practice. In this context, non-small-cell lung cancer (NSCLC) presents clinical, histological and molecular heterogeneity, being one of the most genomically diverse of all cancers. Recent advances added Epidermal Growth Factor Receptor (EGFR) as a predictive biomarker for patients with advanced NSCLC. In tumors with activating EGFR mutations, tyrosine kinase inhibitors (TKI) are indicated as first-line treatment, although restricted to a very small target population. In this context, cofilin-1 (a cytosolic protein involved with actin dynamics) has been widely studied as a biomarker of an aggressive phenotype in tumors, and overexpression of cofilin-1 is associated with cisplatin resistance and poor prognosis in NSCLC. Here, we gather information about the predictive potential of cofilin-1 and reviewed the crosstalk between cofilin-1/EGFR pathways. We aimed to highlight new perspectives of how these interactions might affect cisplatin resistance in NSCLC. We propose that cofilin-1 quantification in clinical samples in combination with presence/absence of EGFR mutation could be used to select patients that would benefit from TKI's treatment. This information is of paramount importance and could result in a possibility of guiding more effective treatments to NSCLC patients.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCisplatinCofilin 1Drug Resistance, NeoplasmErbB ReceptorsHumansLung NeoplasmsMiceSignal TransductionCisplatinCofilin 1ErbB Receptors

Identifiers

PMID25784483
PMCPMC4414134
OpenAlexW1581693885

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.