Evidence map›Paper›PMID 37938738›Full record

ReviewNature reviews. Genetics2024

Scrambling the genome in cancer: causes and consequences of complex chromosome rearrangements.

Ksenia Krupina, Alexander Goginashvili, Don W Cleveland

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  13. A Model for the Diversity Explosion Fundamental to Metastasis.bioRxiv : the preprint server for biology · 2025
    Article
  14. Article
  15. Review
  16. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
  17. Article
  18. Article
  19. Review
  20. TONSL promotes lung adenocarcinoma progression, immune escape and drug sensitivity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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

3 authors at 1 institution in 1 country.

Ksenia Krupina *Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA, USA.
Alexander Goginashvili *Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA, USA.ORCID http://orcid.org/0000-0002-3305-5898
Don W ClevelandDepartment of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA, USA. dcleveland@health.ucsd.edu.ORCID http://orcid.org/0000-0002-1934-3682
University of California San Diego · US

Funding

Mechanisms of chromosome segregation, aneuploidy, and tumorigenesisR35GM122476 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Don W Cleveland · 2017 to 2026
$9.0M
NIGMS NIH HHS R35 GM122476
6 · The paper itself

Abstract

Complex chromosome rearrangements, known as chromoanagenesis, are widespread in cancer. Based on large-scale DNA sequencing of human tumours, the most frequent type of complex chromosome rearrangement is chromothripsis, a massive, localized and clustered rearrangement of one (or a few) chromosomes seemingly acquired in a single event. Chromothripsis can be initiated by mitotic errors that produce a micronucleus encapsulating a single chromosome or chromosomal fragment. Rupture of the unstable micronuclear envelope exposes its chromatin to cytosolic nucleases and induces chromothriptic shattering. Found in up to half of tumours included in pan-cancer genomic analyses, chromothriptic rearrangements can contribute to tumorigenesis through inactivation of tumour suppressor genes, activation of proto-oncogenes, or gene amplification through the production of self-propagating extrachromosomal circular DNAs encoding oncogenes or genes conferring anticancer drug resistance. Here, we discuss what has been learned about the mechanisms that enable these complex genomic rearrangements and their consequences in cancer.

Indexed as

ChromothripsisNeoplasmsCell NucleusChromatinChromosome AberrationsDNAGene RearrangementHumansChromatinDNA

Identifiers

PMID37938738
PMCPMC10922386
OpenAlexW4388490374

What OpenQuestion holds

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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.