Evidence map›Paper›PMID 28899600›Full record

ReviewTrends in cell biology2017

Rebuilding Chromosomes After Catastrophe: Emerging Mechanisms of Chromothripsis.

Peter Ly, Don W Cleveland

Abstract readReview
In one paragraph

Review in Trends in cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 1 pooled it
–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

131 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Cell confinement initiates a delayed but heritable loss of chromosomes.bioRxiv : the preprint server for biology · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Chromothripsis in cancer.Nature reviews. Cancer · 2025
    Review
  17. Review
  18. Chromoanagenesis and Beyond: Catastrophic Events Shaping the Genome.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  19. Chromothripsis.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  20. Review

71 more citing papers are in PubMed but not listed here.

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

2 authors.

Peter LyLudwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA. Electronic address: p3ly@ucsd.edu.
Don W ClevelandLudwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA. Electronic address: dcleveland@ucsd.edu.

Funding

Mechanisms of chromosome segregation, aneuploidy, and tumorigenesisR35GM122476 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Don W Cleveland · 2017 to 2026
$9.0M
Cell Division Errors as a Mechanism Driving Massive Genomic RearrangementsK99CA218871 · NCI · LUDWIG INSTITUTE FOR CANCER RES LTD · PI LY, PETER · 2017 to 2018
$236k
NCI NIH HHS K99 CA218871NIGMS NIH HHS R35 GM122476
6 · The paper itself

Abstract

Cancer genome sequencing has identified chromothripsis, a complex class of structural genomic rearrangements involving the apparent shattering of an individual chromosome into tens to hundreds of fragments. An initial error during mitosis, producing either chromosome mis-segregation into a micronucleus or chromatin bridge interconnecting two daughter cells, can trigger the catastrophic pulverization of the spatially isolated chromosome. The resultant chromosomal fragments are religated in random order by DNA double-strand break repair during the subsequent interphase. Chromothripsis scars the cancer genome with localized DNA rearrangements that frequently generate extensive copy number alterations, oncogenic gene fusion products, and/or tumor suppressor gene inactivation. Here we review emerging mechanisms underlying chromothripsis with a focus on the contribution of cell division errors caused by centromere dysfunction.

Indexed as

ChromothripsisDNA Breaks, Double-StrandedDNA RepairCentromereChromatinDNAGenome, HumanHumansMitosisModels, GeneticChromatinDNAchromosome rearrangementschromothripsisDNA repairgenomic instabilitymicronucleimitosis

Identifiers

PMID28899600
PMCPMC5696049

What OpenQuestion holds

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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.