Evidence map›Paper›PMID 25351872›Full record

ArticleMolecular medicine reports2015

Identification of differential splicing genes in gliomas using exon expression profiling.

Feng Yu, Wei-Ming Fu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
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

2 authors at 1 institution in 1 country.

Feng YuDepartment of Neurosurgery, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China.
Wei-Ming FuDepartment of Neurosurgery, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse gliomas are the most common type of malignant primary brain tumor, and their initiation and/or progression are often associated with alternative splicing. They produce an enormous economic burden on society and greatly impair the quality of life of those affected. The aim of the current study was to explore the differentially expressed genes (DEGs) observed in glioblastoma (GBM) and oligodendroglioma (OD) at the splicing level, and to analyze their functions in order to identify the underlying molecular mechanisms of gliomas. The exon‑level expression profile data GSE9385 was downloaded from the Gene Expression Omnibus database, and included 26 GBM samples, 22 OD samples and 6 control brain samples. The differentially expressed exon‑level probes were analyzed using the microarray detection of alternative splicing algorithm combined with the splicing index method, and the corresponding DEGs were identified. Next, a Gene Ontology enrichment analysis of the DEGs was performed. Additionally, the protein‑protein interaction (PPI) networks were constructed based on the depth‑first search algorithm. A total of 300 DEGs were identified to be shared by GBM and OD, including 97 upregulated and 203 downregulated DEGs. Furthermore, screening with a defined threshold identified 6 genes that were highly expressed in GBM, including AFF2, CACNA2D3 and ARPP21, while the 6 highly expressed genes in OD notably included CNTN2. The TP53 and HIST1H3A genes were the hub nodes in the PPI network of DEGs from GBM, while CNTN2 was linked to the highest degree in the OD PPI network. The present study provides a comprehensive bioinformatics analysis of DEGs in GBM and OD, which may provide a basis for understanding the initiation and/or progression of glioma development.

Indexed as

Gene Expression ProfilingBrain NeoplasmsCalcium ChannelsContactin 2Down-RegulationExonsGliomaHistonesHumansNuclear ProteinsOligonucleotide Array Sequence AnalysisPhosphoproteinsProtein Interaction MapsTumor Suppressor Protein p53Up-RegulationAFF2 protein, humanCACNA2D3 protein, humanCalcium ChannelsCNTN2 protein, humanContactin 2cyclic AMP-regulated phosphoprotein ARPP-21HistonesNuclear ProteinsPhosphoproteinsTumor Suppressor Protein p53

Identifiers

PMID25351872
PMCPMC4262513
OpenAlexW2017269626

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.