Evidence map›Paper›PMID 34120190›Full record

ReviewNeuro-oncology2021

The role of human endogenous retroviruses in gliomas: from etiological perspectives and therapeutic implications.

Ashish H Shah, Mark Gilbert, Michael E Ivan, Ricardo J Komotar, John Heiss, Avindra Nath

Open access · bronzeAbstract readReview
In one paragraph

Review in Neuro-oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  8. Cancer Vaccines: Recent Insights and Future Directions.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Trophoblast PR-SET7 dysfunction induces viral mimicry response and necroptosis associated with recurrent miscarriage.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Review
  13. 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

6 authors at 3 institutions in 1 country.

Ashish H ShahDepartment of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.ORCID 0000-0002-0183-1274
Mark GilbertNeuro-oncology Branch, National Cancer Institute, National Institute of Health, Bethesda, Maryland, USA.
Michael E IvanDepartment of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.ORCID 0000-0002-4798-4989
Ricardo J KomotarDepartment of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.ORCID 0000-0002-7626-8869
John HeissSurgical Neurology Branch, NINDS, NIH, Bethesda, Maryland, USA.
Avindra NathTranslational Neuroscience Center, NINDS, NIH, Bethesda, Maryland, USA.ORCID 0000-0003-0927-5855
University of Miami · USNational Institutes of Health · USNational Cancer Institute · US

Funding

Molecular Pathogenesis of NeoplasiaZIANS003052 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI HEISS, JOHN · 2009 to 2025
$20.7M
University of MIami Neurosurgery eDucation Strategy UMINDSR25NS108937 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DIETRICH, W DALTON, IAVARONE, ANTONIO · 2019 to 2024
$558k
NINDS NIH HHS R25 NS108937
6 · The paper itself

Abstract

Accounting for approximately 8% of the human genome, human endogenous retroviruses (HERVs) have been implicated in a variety of cancers including gliomas. In normal cells, tight epigenetic regulation of HERVs prevent aberrant expression; however, in cancer cells, HERVs expression remains pervasive, suggesting a role of HERVs in oncogenic transformation. HERVs may contribute to oncogenesis in several ways including insertional mutagenesis, chromosomal rearrangements, proto-oncogene formation, and maintenance of stemness. On the other hand, recent data has suggested that reversing epigenetic silencing of HERVs may induce robust anti-tumor immune responses, suggesting HERVs' potential therapeutic utility in gliomas. By reversing epigenetic modifications that silence HERVs, DNA methyltransferase, and histone deacetylase inhibitors may stimulate a viral-mimicry cascade via HERV-derived dsRNA formation that induces interferon-mediated apoptosis. Leveraging this anti-tumor autoimmune response may be a unique avenue to target certain subsets of epigenetically-dysregulated gliomas. Nevertheless, the role of HERVs in gliomas as either arbitrators of oncogenesis or forerunners of the innate anti-tumor immune response remains unclear. Here, we review the role of HERVs in gliomas, their potential dichotomous function in propagating oncogenesis and stimulating the anti-tumor immune response, and identify future directions for research.

Indexed as

Endogenous RetrovirusesGliomaCarcinogenesisEpigenesis, GeneticHumansProto-Oncogene MasProto-Oncogene Masetiologygliomahuman endogenous retrovirusviral mimicry

Identifiers

PMID34120190
PMCPMC8485438
OpenAlexW3172516882

What OpenQuestion holds

Textmetadata
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.