Evidence map›Paper›PMID 23759584›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Chromothripsis: breakage-fusion-bridge over and over again.

Carlos Oscar Sánchez Sorzano, Alberto Pascual-Montano, Ainhoa Sánchez de Diego, Carlos Martínez-A, Karel H M van Wely

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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  17. Review
  18. The elusive evidence for chromothripsis.Nucleic acids research · 2014
    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.

Carlos Oscar Sánchez SorzanoBiocomputation Group, Centro Nacional de Biotecnología-CSIC, Madrid, Spain.
Alberto Pascual-Montano
Ainhoa Sánchez de Diego
Carlos Martínez-A
Karel H M van Wely

Funding

NIMHD NIH HHS L60 MD002502
6 · The paper itself

Abstract

The acquisition of massive but localized chromosome translocations, a phenomenon termed chromothripsis, has received widespread attention since its discovery over a year ago. Until recently, chromothripsis was believed to originate from a single catastrophic event, but the molecular mechanisms leading to this event are yet to be uncovered. Because a thorough interpretation of the data are missing, the phenomenon itself has wrongly acquired the status of a mechanism used to justify many kinds of complex rearrangements. Although the assumption that all translocations in chromothripsis originate from a single event has met with criticism, satisfactory explanations for the intense but localized nature of this phenomenon are still missing. Here, we show why the data used to describe massive catastrophic rearrangements are incompatible with a model comprising a single event only and propose a molecular mechanism in which a combination of known cellular pathways accounts for chromothripsis. Instead of a single traumatic event, the protection of undamaged chromosomes by telomeres can limit repetitive breakage-fusion-bridge events to a single chromosome arm. Ultimately, common properties of chromosomal instability, such as aneuploidy and centromere fission, might establish the complex genetic pattern observed in this genomic state.

Indexed as

Translocation, GeneticChromosomal InstabilityChromosome BreakageChromosomes, HumanDNA FragmentationDNA RepairHumansModels, GeneticTelomerebreakage-fusion-bridgecentromere fissionchromosomal instabilitychromothripsismitosistelomere

Identifiers

PMID23759584
PMCPMC3737304

What OpenQuestion holds

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Registered trials

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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.