Evidence map›Paper›PMID 33479235›Full record

ArticleNature communications2021

Oncogenic herpesvirus KSHV triggers hallmarks of alternative lengthening of telomeres.

Timothy P Lippert, Paulina Marzec, Aurora I Idilli, Grzegorz Sarek, Aleksandra Vancevska, Mark Bower, Paul J Farrell, Päivi M Ojala, Niklas Feldhahn, Simon J Boulton

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  5. Anellovirus protein encoded byProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025
    Review
  7. Review
  8. Review
  9. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
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  11. Review
  12. Review
  13. Article
  14. Article
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  16. Review
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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

10 authors at 5 institutions in 2 countries.

Timothy P LippertThe Francis Crick Institute, 1 Midland Road, London, NW11AT, UK.
Paulina MarzecThe Francis Crick Institute, 1 Midland Road, London, NW11AT, UK.ORCID 0000-0002-4081-7539
Aurora I IdilliThe Francis Crick Institute, 1 Midland Road, London, NW11AT, UK.ORCID 0000-0002-5011-0553
Grzegorz SarekThe Francis Crick Institute, 1 Midland Road, London, NW11AT, UK.
Aleksandra VancevskaThe Francis Crick Institute, 1 Midland Road, London, NW11AT, UK.
Mark BowerNational Centre for HIV Malignancy, Department of Oncology, Chelsea & Westminster Hospital, Fulham Road, London, SW10 9NH, UK.
Paul J FarrellSection of Virology, Department of Infectious Diseases, Imperial College London, Norfolk Place, London, W2 1PG, UK.
Päivi M OjalaSection of Virology, Department of Infectious Diseases, Imperial College London, Norfolk Place, London, W2 1PG, UK.ORCID 0000-0001-9065-1832
Niklas Feldhahn *Department of Immunology & Inflammation, Centre for Haematology, Du Cane Road, London, W12 0NN, UK.ORCID 0000-0002-9132-0880
Simon J Boulton *The Francis Crick Institute, 1 Midland Road, London, NW11AT, UK. simon.boulton@crick.ac.uk.ORCID 0000-0001-6936-6834
The Francis Crick Institute · GBCentre for Inflammation Research · GBChelsea and Westminster Hospital · GBImperial College London · GBUniversity of Helsinki · FI

Funding

Cancer Research UK FC0010048Department of HealthMedical Research Council FC0010048Medical Research Council MR/S022597/1Wellcome TrustWellcome Trust FC0010048
6 · The paper itself

Abstract

To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which relies on break-induced replication (BIR) and telomere recombination. Although ALT tumours were first reported over 20 years ago, the mechanism of ALT induction remains unclear and no study to date has described a cell-based model that permits the induction of ALT. Here, we demonstrate that infection with Kaposi's sarcoma herpesvirus (KSHV) induces sustained acquisition of ALT-like features in previously non-ALT cell lines. KSHV-infected cells acquire hallmarks of ALT activity that are also observed in KSHV-associated tumour biopsies. Down-regulating BIR impairs KSHV latency, suggesting that KSHV co-opts ALT for viral functionality. This study uncovers KSHV infection as a means to study telomere maintenance by ALT and reveals features of ALT in KSHV-associated tumours.

Indexed as

CarcinogenesisCell LineCell Line, TumorDNA DamageDNA ReplicationHeLa CellsHerpesvirus 8, HumanHost-Pathogen InteractionsHumansIn Situ Hybridization, FluorescenceNeoplasmsProteomeTelomeraseTelomereTelomere HomeostasisTelomere ShorteningProteomeTelomerase

Identifiers

PMID33479235
PMCPMC7820467
OpenAlexW3125793489

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.