Evidence map›Paper›PMID 29845785›Full record

ArticleCell journal2018

Chronic Obstructive Pulmonary Disease Molecular Subtyping and Pathway Deviation-Based Candidate Gene Identification.

Jingming Zhao, Wei Cheng, Xigang He, Yanli Liu, Ji Li, Jiaxing Sun, Jinfeng Li, Fangfang Wang, Yufang Gao

Abstract read
In one paragraph

Article in Cell journal, 2018. 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
–field-weighted citation impact
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.

  1. Integrative multi-omics identifies CYP1B1 as a candidate molecular link between toxicant exposure and ferroptosis-related epithelial stress in COPD.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Review
  3. Article
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  5. Review
  6. Identification of Small Airway Epithelium-Related Hub Genes in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2022
    Article
  7. Article
  8. Article
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  10. Article
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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

9 authors.

Jingming ZhaoDepartment of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Wei ChengDepartment of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Xigang HeDepartment of Respiratory Medicine, People's Hospital of RizhaoLanshan, Rizhao, China.
Yanli LiuDepartment of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Ji LiDepartment of Pharmacy, Qilu Hospital of Shandong University (Qingdao), Qingdao, China.
Jiaxing SunDepartment of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Jinfeng LiDepartment of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Fangfang WangDepartment of Respiratory Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Yufang GaoDepartment of President's Office, The Affiliated Hospital of Qingdao University, Qingdao, China.Electronic Address: gaoyufang201508@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aim of this study was to identify the molecular subtypes of chronic obstructive pulmonary disease (COPD) and to prioritize COPD candidate genes using bioinformatics methods. MATERIALS AND

methodsIn this bioinformatics study, the gene expression dataset GSE76705 (including 229 COPD samples) and known COPD-related genes (candidate genes) were downloaded from the Gene Expression Omnibus (GEO) and the Online Mendelian Inheritance in Man (OMIM) databases respectively. Based on the expression values of the candidate genes, COPD samples were divided into molecular subtypes through hierarchical clustering analysis. Candidate genes were accordingly allocated into the defined molecular subtypes and functional enrichment analysis was undertaken. Pathway deviation scores were then analyzed, followed by the analysis of clinical indicators (FEV1, FEV1/FVC, age and gender) of COPD patients in each subtype, and prediction models were constructed. Furthermore, the gene expression dataset GSE71220 was used to bioinformatically validate our results.

resultsA total of 213 COPD-related genes were identified, which divided samples into three subtypes based on the gene expression values. After intersection analysis, 160 common genes including transforming growth factor β1 (TGFB1), epidermal growth factor receptor (EGFR) and interleukin 13 (IL13) were obtained. Functional enrichment analysis identified 22 pathways such as 'hsa04060: cytokine-cytokine receptor interaction pathways, 'hsa04110: cell cycle' and 'hsa05222: small cell lung cancer'. Pathways in subtype 2 had higher deviation scores. Furthermore, three receiver operating characteristic (ROC) curves (accuracies >80%) were constructed. The three subtypes in COPD samples were also identified in the validation dataset GSE71220.

conclusionCOPD may be further subdivided into several molecular subtypes, which may be useful in improving COPD therapy based on the molecular subtype of a patient.

Indexed as

Chronic Obstructive Pulmonary DiseasePathwaySubtype

Identifiers

PMID29845785
PMCPMC6004990

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