Evidence map›Paper›PMID 31333911›Full record

ArticlePeerJ2019

Bioinformatics analysis of microarray data to identify the candidate biomarkers of lung adenocarcinoma.

Tingting Guo, Hongtao Ma, Yubai Zhou

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.8field-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

30 citing papers in PubMed, 64 citations in OpenAlex.

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  11. Identification of a Novel Risk Model: A Five-Gene Prognostic Signature for Pancreatic Cancer.Evidence-based complementary and alternative medicine : eCAM · 2022
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  13. An Immune-Related Prognostic Risk Model in Colon Cancer by Bioinformatics Analysis.Evidence-based complementary and alternative medicine : eCAM · 2022
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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

3 authors at 1 institution in 1 country.

Tingting Guo *Department of Biotechnology, College of Life Science & Bioengineering, Beijing University of Technology, Beijing, China.
Hongtao Ma *Department of Biotechnology, College of Life Science & Bioengineering, Beijing University of Technology, Beijing, China.
Yubai ZhouDepartment of Biotechnology, College of Life Science & Bioengineering, Beijing University of Technology, Beijing, China.
Beijing University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is the major subtype of lung cancer and the most lethal malignant disease worldwide. However, the molecular mechanisms underlying LUAD are not fully understood.

methodsFour datasets (GSE118370, GSE85841, GSE43458 and GSE32863) were obtained from the gene expression omnibus (GEO). Identification of differentially expressed genes (DEGs) and functional enrichment analysis were performed using the limma and clusterProfiler packages, respectively. A protein-protein interaction (PPI) network was constructed via Search Tool for the Retrieval of Interacting Genes (STRING) database, and the module analysis was performed by Cytoscape. Then, overall survival analysis was performed using the Kaplan-Meier curve, and prognostic candidate biomarkers were further analyzed using the Oncomine database.

resultsTotally, 349 DEGs were identified, including 275 downregulated and 74 upregulated genes which were significantly enriched in the biological process of extracellular structure organization, leukocyte migration and response to peptide. The mainly enriched pathways were complement and coagulation cascades, malaria and prion diseases. By extracting key modules from the PPI network, 11 hub genes were screened out. Survival analysis showed that except VSIG4, other hub genes may be involved in the development of LUAD, in which MYH10, METTL7A, FCER1G and TMOD1 have not been reported previously to correlated with LUAD. Briefly, novel hub genes identified in this study will help to deepen our understanding of the molecular mechanisms of LUAD carcinogenesis and progression, and to discover candidate targets for early detection and treatment of LUAD.

Indexed as

Bioinformatical analysisBiomarkerDifferentially expressed genesLung adenocarcinomaMicroarray

Identifiers

PMID31333911
PMCPMC6626531
OpenAlexW2958836234

What OpenQuestion holds

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LicenceCC BY
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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.