Evidence map›Paper›PMID 29890994›Full record

ArticleActa neuropathologica communications2018

Network-based analysis of oligodendrogliomas predicts novel cancer gene candidates within the region of the 1p/19q co-deletion.

Josef Gladitz, Barbara Klink, Michael Seifert

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Oligodendrocyte-specific expression ofNon-coding RNA research · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. ELTD1-An Emerging Silent Actor in Cancer Drama Play.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Review
  15. LncRNACancer management and research · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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 2 institutions in 1 country.

Josef GladitzInstitute for Medical Informatics and Biometry, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Barbara KlinkInstitute for Clinical Genetics, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
Michael SeifertInstitute for Medical Informatics and Biometry, Carl Gustav Carus Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. michael.seifert@tu-dresden.de.
National Center for Tumor Diseases · DETU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oligodendrogliomas are primary human brain tumors with a characteristic 1p/19q co-deletion of important prognostic relevance, but little is known about the pathology of this chromosomal mutation. We developed a network-based approach to identify novel cancer gene candidates in the region of the 1p/19q co-deletion. Gene regulatory networks were learned from gene expression and copy number data of 178 oligodendrogliomas and further used to quantify putative impacts of differentially expressed genes of the 1p/19q region on cancer-relevant pathways. We predicted 8 genes with strong impact on signaling pathways and 14 genes with strong impact on metabolic pathways widespread across the region of the 1p/19 co-deletion. Many of these candidates (e.g. ELTD1, SDHB, SEPW1, SLC17A7, SZRD1, THAP3, ZBTB17) are likely to push, whereas others (e.g. CAP1, HBXIP, KLK6, PARK7, PTAFR) might counteract oligodendroglioma development. For example, ELTD1, a functionally validated glioblastoma oncogene located on 1p, was overexpressed. Further, the known glioblastoma tumor suppressor SLC17A7 located on 19q was underexpressed. Moreover, known epigenetic alterations triggered by mutated SDHB in paragangliomas suggest that underexpressed SDHB in oligodendrogliomas may support and possibly enhance the epigenetic reprogramming induced by the IDH-mutation. We further analyzed rarely observed deletions and duplications of chromosomal arms within oligodendroglioma subcohorts identifying putative oncogenes and tumor suppressors that possibly influence the development of oligodendroglioma subgroups. Our in-depth computational study contributes to a better understanding of the pathology of the 1p/19q co-deletion and other chromosomal arm mutations. This might open opportunities for functional validations and new therapeutic strategies.

Indexed as

Chromosome DeletionBrain NeoplasmsChromosomes, Human, Pair 1Chromosomes, Human, Pair 19Computational BiologyFemaleGene DosageGene Expression Regulation, NeoplasticHumansIsocitrate DehydrogenaseMaleMetabolic Networks and PathwaysMutationNeoplasm ProteinsOligodendrogliomaSignal TransductionIDH1 protein, humanIsocitrate DehydrogenaseNeoplasm ProteinsSDHB protein, humanSLC17A7 protein, humanSuccinate DehydrogenaseVesicular Glutamate Transport Protein 11p/19q co-deletionBioinformaticsCancer genomicsComputational systems biologyNetwork biologyNetwork inferenceNetwork propagationOligodendrogliomas

Identifiers

PMID29890994
PMCPMC5996550
OpenAlexW2808522237

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.