Evidence map›Paper›PMID 30132538›Full record

ArticleMolecular medicine reports2018

Bioinformatics analyses of significant genes, related pathways and candidate prognostic biomarkers in glioblastoma.

Lingqi Zhou, Hai Tang, Fang Wang, Lizhi Chen, Shanshan Ou, Tong Wu, Jie Xu, Kaihua Guo

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 3 pooled it
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

43 citing papers in PubMed, 3 syntheses or guidelines pooled it, 58 citations in OpenAlex.

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  18. The Journal of international medical research · 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

8 authors at 2 institutions in 1 country.

Lingqi ZhouDepartment of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Hai TangDepartment of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Fang WangDepartment of Molecular Diagnostics, Sun Yat‑sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.
Lizhi ChenDepartment of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Shanshan OuDepartment of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Tong WuDepartment of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Jie XuDepartment of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Kaihua GuoDepartment of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common type of malignant tumor of the central nervous system. The prognosis of patients with GBM is very poor, with a survival time of ~15 months. GBM is highly heterogeneous and highly aggressive. Surgical removal of intracranial tumors does provide a good advantage for patients as there is a high rate of recurrence. The understanding of this type of cancer needs to be strengthened, and the aim of the present study was to identify gene signatures present in GBM and uncover their potential mechanisms. The gene expression profiles of GSE15824 and GSE51062 were downloaded from the Gene Expression Omnibus database. Normalization of the data from primary GBM samples and normal samples in the two databases was conducted using R software. Then, joint analysis of the data was performed. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed, and the protein‑protein interaction (PPI) network of the differentially expressed genes (DEGs) was constructed using Cytoscape software. Identification of prognostic biomarkers was conducted using UALCAN. In total, 9,341 DEGs were identified in the GBM samples, including 9,175 upregulated genes and 166 downregulated genes. The top 1,000 upregulated DEGs and all of the downregulated DEGs were selected for GO, KEGG and prognostic biomarker analyses. The GO results showed that the upregulated DEGs were significantly enriched in biological processes (BP), including immune response, cell division and cell proliferation, and the downregulated DEGs were also significantly enriched in BP, including cell growth, intracellular signal transduction and signal transduction by protein phosphorylation. KEGG pathway analysis showed that the upregulated DEGs were enriched in circadian entrainment, cytokine‑cytokine receptor interaction and maturity onset diabetes of the young, while the downregulated DEGs were enriched in the TGF‑β signaling pathway, MAPK signaling pathway and pathways in cancer. All of the downregulated genes and the top 1,000 upregulated genes were selected to establish the PPI network, and the sub‑networks revealed that these genes were involved in significant pathways, including olfactory transduction, neuroactive ligand‑receptor interaction and viral carcinogenesis. In total, seven genes were identified as good prognostic biomarkers. In conclusion, the identified DEGs and hub genes contribute to the understanding of the molecular mechanisms underlying the development of GBM and they may be used as diagnostic and prognostic biomarkers and molecular targets for the treatment of patients with GBM in the future.

Indexed as

Computational BiologyGene Expression Regulation, NeoplasticGene Regulatory NetworksSignal TransductionTranscriptomeBiomarkersGene Expression ProfilingGene OntologyGlioblastomaHumansPrognosisProtein Interaction MappingProtein Interaction MapsBiomarkers

Identifiers

PMID30132538
PMCPMC6172372
OpenAlexW2888221369

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.