Evidence map›Paper›PMID 30872351›Full record

ArticleGenome research2019

Chromothripsis during telomere crisis is independent of NHEJ, and consistent with a replicative origin.

Kez Cleal, Rhiannon E Jones, Julia W Grimstead, Eric A Hendrickson, Duncan M Baird

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed, 59 citations in OpenAlex.

  1. How telomere attrition protects against cancer.Nature reviews. Genetics · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Chromoanasynthesis.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. 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

5 authors at 2 institutions in 2 countries.

Kez ClealDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff, CF14 4XN, United Kingdom.
Rhiannon E JonesDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff, CF14 4XN, United Kingdom.
Julia W GrimsteadDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff, CF14 4XN, United Kingdom.
Eric A HendricksonDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.
Duncan M BairdDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff, CF14 4XN, United Kingdom.ORCID 0000-0001-8408-5467
Cardiff University · GBUniversity of Minnesota Medical Center · US

Funding

The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cellsR01GM088351 · NIGMS · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2010 to 2018
$2.3M
Ligase III regulates survival from crisis induced by gradual telomere shorteningR01CA190492 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2015 to 2019
$1.7M
Ku regulates non-homologous end joining pathways in human somatic cellsR01CA154461 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2011 to 2015
$1.6M
Cancer Research UK 17199/A18246Cancer Research UK 18246NCI NIH HHS R01 CA154461NCI NIH HHS R01 CA190492NIGMS NIH HHS R01 GM088351
6 · The paper itself

Abstract

Telomere erosion, dysfunction, and fusion can lead to a state of cellular crisis characterized by large-scale genome instability. We investigated the impact of a telomere-driven crisis on the structural integrity of the genome by undertaking whole-genome sequence analyses of clonal populations of cells that had escaped crisis. Quantification of large-scale structural variants revealed patterns of rearrangement consistent with chromothripsis but formed in the absence of functional nonhomologous end-joining pathways. Rearrangements frequently consisted of short fragments with complex mutational patterns, with a repair topology that deviated from randomness showing preferential repair to local regions or exchange between specific loci. We find evidence of telomere involvement with an enrichment of fold-back inversions demarcating clusters of rearrangements. Our data suggest that chromothriptic rearrangements caused by a telomere crisis arise via a replicative repair process involving template switching.

Indexed as

ChromothripsisGenomic InstabilityChromosome InversionDNA Copy Number VariationsDNA End-Joining RepairGenomic Structural VariationHCT116 CellsHumansMutationNeoplasmsReplication OriginTelomereWhole Genome Sequencing

Identifiers

PMID30872351
PMCPMC6499312
OpenAlexW2922503170

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.