Evidence map›Paper›PMID 40884659›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2025

Transcription-Replication Conflicts and Incomplete Replication as a Cause of Micronuclei-Driven Chromoanagenesis.

Hervé Técher, Philippe Pasero

Abstract read
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In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Hervé TécherUniversité Côte d'Azur, Institute for Research on Cancer and Aging of Nice (IRCAN), CNRS, INSERM, Nice, France. herve.techer@univ-cotedazur.fr.
Philippe PaseroInstitut de Génétique Humaine, Université de Montpellier, CNRS, Equipe Labellisée Ligue contre le Cancer, Montpellier, France. philippe.pasero@igh.cnrs.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancers are characterized with altered genomes. Sequencing of thousands of cancer genomes has led to the identification of new types of complex genomic rearrangements that generate new chromosomes, known as chromoanagenesis. Chromothripsis is, to-date, the best characterized phenomenon of complex rearrangements, in which a single chromosome pulverization is followed by reassembly of broken DNA fragments in a random manner. Chromothripsis and chromothripsis-related events predominantly stem from mitotic- and post-mitotic aberrations, notably in consequence of chromatin bridges and micronuclei breakage. These mitotic defects result either from DNA breaks or from perturbations in the DNA replication program, leading to under-replication and DNA damage. In this chapter we describe the molecular mechanisms that connect replication stress to chromothripsis-related events. We focus on transcription-replication conflicts as a major source of endogenous replication stress.

Indexed as

ChromothripsisDNA ReplicationMicronuclei, Chromosome-DefectiveTranscription, GeneticDNA DamageHumansMitosisNeoplasmsCancerChromothripsisDNA breaksMicronucleiMitotic bridgesReplication stressRNaseH2Transcription-replication conflictsTREX1

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.