Evidence map›Paper›PMID 35477752›Full record

ArticleScientific reports2022

Differential expression of an endogenous retroviral element [HERV-K(HML-6)] is associated with reduced survival in glioblastoma patients.

Ashish H Shah, Vaidya Govindarajan, Tara T Doucet-O'Hare, Sarah Rivas, Leo Ampie, Catherine DeMarino, Yeshavanth Kumar Banasavadi-Siddegowda, Yong Zhang, Kory R Johnson, Fahad Almsned and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.8field-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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

13 authors at 4 institutions in 1 country.

Ashish H Shah *Surgical Neurology Branch, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA. ashish.shah2@nih.gov.
Vaidya Govindarajan *Department of Neurosurgery, University of Miami School of Medicine, Miami, FL, USA.
Tara T Doucet-O'HareCenter for Cancer Research (CCR), National Institutes of Health, National Cancer Institute (NCI), Neuro-Oncology Branch (NOB), Bethesda, MD, USA.
Sarah RivasSurgical Neurology Branch, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Leo AmpieSurgical Neurology Branch, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Catherine DeMarinoSurgical Neurology Branch, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Yeshavanth Kumar Banasavadi-SiddegowdaSurgical Neurology Branch, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Yong ZhangBioinformatics Section, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Kory R JohnsonBioinformatics Section, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Fahad AlmsnedBioinformatics Section, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Mark R GilbertCenter for Cancer Research (CCR), National Institutes of Health, National Cancer Institute (NCI), Neuro-Oncology Branch (NOB), Bethesda, MD, USA.
John D HeissSurgical Neurology Branch, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
Avindra NathSurgical Neurology Branch, National Institutes of Health, National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, MD, USA.
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · USCenter for Cancer Research · USUniversity of Miami · US

Funding

Neuropathogenesis of Retroviral InfectionsZIANS003130 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI NATH, AVINDRA · 2011 to 2025
$73.7M
Brain Tumor Clinical and Clinical Research Program (Clinical Support Services)ZIDBC011642 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI OZER, BYRAM · 2015 to 2025
$23.4M
Molecular Pathogenesis of NeoplasiaZIANS003052 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI HEISS, JOHN · 2009 to 2025
$20.7M
Bioinformatics Core Facility ZICNS009443 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI JOHNSON, KORY · 2022 to 2025
$8.5M
6 · The paper itself

Abstract

Comprising approximately 8% of our genome, Human Endogenous RetroViruses (HERVs) represent a class of germline retroviral infections that are regulated through epigenetic modifications. In cancer cells, which often have epigenetic dysregulation, HERVs have been implicated as potential oncogenic drivers. However, their role in gliomas is not known. Given the link between HERV expression in cancer cell lines and the distinct epigenetic dysregulation in gliomas, we utilized a tailored bioinformatic pipeline to characterize and validate the glioma retrotranscriptome and correlate HERV expression with locus-specific epigenetic modifications. We identified robust overexpression of multiple HERVs in our cell lines, including a retroviral transcript, HML-6, at 19q13.43b in glioblastoma cells. HERV expression inversely correlated with loci-specific DNA methylation. HML-6 contains an intact open reading frame encoding a small envelope protein, ERVK3-1. Increased expression of ERVK3-1 in GBM patients is associated with a poor prognosis independent of IDH-mutational status. Our results suggest that not only is HML-6 uniquely overexpressed in highly invasive cell lines and tissue samples, but also its gene product, ERVK3-1, may be associated with reduced survival in GBM patients. These results may have implications for both the tumor biology of GBM and the role of ERVK3-1 as a potential therapeutic target.

Indexed as

Endogenous RetrovirusesGlioblastomaComputational BiologyDNA MethylationHumansOpen Reading Frames

Identifiers

PMID35477752
PMCPMC9046263
OpenAlexW4225094323

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.