Evidence map›Paper›PMID 29548337›Full record

ReviewJournal of experimental & clinical cancer research : CR2018

The interplay of reactive oxygen species and the epidermal growth factor receptor in tumor progression and drug resistance.

Meng-Shih Weng, Jer-Hwa Chang, Wen-Yueh Hung, Yi-Chieh Yang, Ming-Hsien Chien

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

98 citing papers in PubMed, 171 citations in OpenAlex.

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

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

5 authors at 5 institutions in 1 country.

Meng-Shih WengDepartment of Nutritional Science, Fu Jen Catholic University, New Taipei City, Taiwan.
Jer-Hwa ChangDepartment of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Wen-Yueh HungGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 11031, Taiwan.
Yi-Chieh YangGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 11031, Taiwan.
Ming-Hsien ChienGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 11031, Taiwan. mhchien1976@gmail.com.ORCID http://orcid.org/0000-0002-0084-7231
Fu Jen Catholic University · TWGenomics Research Center, Academia Sinica · TWTaipei Medical University · TWTaipei Medical University Hospital · TWWan Fang Hospital · TW

Funding

Wan Fang Hospital 106TMU-WFH-13
6 · The paper itself

Abstract

backgroundThe epidermal growth factor receptor (EGFR) plays important roles in cell survival, growth, differentiation, and tumorigenesis. Dysregulation of the EGFR is a common mechanism in cancer progression especially in non-small cell lung cancer (NSCLC). MAIN BODY: Suppression of the EGFR-mediated signaling pathway is used in cancer treatment. Furthermore, reactive oxygen species (ROS)-induced oxidative stress from mitochondrial dysfunction or NADPH oxidase (NOX) overactivation and ectopic expression of antioxidative enzymes were also indicated to be involved in EGFR-mediated tumor progression (proliferation, differentiation, migration, and invasion) and drug resistance (EGFR tyrosine kinase inhibitor (TKI)). The products of NOX, superoxide and hydrogen peroxide, are considered to be major types of ROS. ROS are not only toxic materials to cells but also signaling regulators of tumor progression. Oxidation of both the EGFR and downstream phosphatases by ROS enhances EGFR-mediated signaling and promotes tumor progression. This review primarily focuses on the recent literature with respect to the roles of the EGFR and ROS and correlations between ROS and the EGFR in tumor progression and EGFR TKI resistance. SHORT

conclusionThe evidence discussed in this article can serve as a basis for basic and clinical research to understand how to modulate ROS levels to control the development and drug resistance of cancers.

Indexed as

Drug Resistance, NeoplasmAnimalsCarcinoma, Non-Small-Cell LungDisease ProgressionErbB ReceptorsHumansLung NeoplasmsNADPH OxidasesNeoplasmsNeovascularization, PathologicOxidation-ReductionOxidative StressProtein Kinase InhibitorsReactive Oxygen SpeciesSignal TransductionEGFR protein, humanErbB ReceptorsNADPH OxidasesProtein Kinase InhibitorsReactive Oxygen SpeciesDrug resistanceEpidermal growth factor receptorNADPH oxidaseOxidationReactive oxygen speciesTumor progression

Identifiers

PMID29548337
PMCPMC5857086
OpenAlexW2801669720

What OpenQuestion holds

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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.