ReviewChromosoma2020
Understanding the birth of rupture-prone and irreparable micronuclei.
Review in Chromosoma, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 44 citations in OpenAlex.
- Barrier-to-autointegration factor protects against the cGAS-STING response to chromatin bridges.PLoS genetics · 2026Article
- Aneuploidy in exfoliated buccal cells: mechanisms, methods, and future perspectives.Mutagenesis · 2026Review
- Unclassified Chromosomal Abnormalities as an Indicator of Genomic Damage in Survivors of Hodgkin's Lymphoma.Cancers · 2025Article
- Neutrophils secrete exosome-associated DNA to resolve sterile acute inflammation.Nature cell biology · 2025Article
- Article
- Perspectives on Ergodic Cancer Therapy Derived from Cloning Genome ChaosCurrent cancer drug targets · 2025Review
- High prevalence of chromosome 17 in breast cancer micronuclei: a means to get rid of tumor suppressors?Human cell · 2024Article
- Nuclear reassembly defects after mitosis trigger apoptotic and p53-dependent safeguard mechanisms in Drosophila.PLoS biology · 2024Article
- Arabidopsis AN3 and OLIGOCELLULA genes link telomere maintenance mechanisms with cell division and expansion control.Plant molecular biology · 2024Article
- Article
- Cytoplasmic DNA and AIM2 inflammasome in RA: where they come from and where they go?Frontiers in immunology · 2024Review
- Arabidopsis AN3 and OLIGOCELLULA genes link telomere maintenance mechanisms with cell division and expansion control.Research square · 2023Article
- The multifaceted functions of cGAS.Journal of molecular cell biology · 2022Review
- Review
- The chromatin-binding domain of Ki-67 together with p53 protects human chromosomes from mitotic damage.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- ER Stress and Micronuclei Cluster: Stress Response Contributes to Genome Chaos in Cancer.Frontiers in cell and developmental biology · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Micronuclei are extra-nuclear bodies mainly derived from ana-telophase lagging chromosomes/chromatins (LCs) that are not incorporated into primary nuclei at mitotic exit. Unlike primary nuclei, most micronuclei are enclosed by nuclear envelope (NE) that is highly susceptible to spontaneous and irreparable rupture. Ruptured micronuclei act as triggers of chromothripsis-like chaotic chromosomal rearrangements and cGAS-mediated innate immunity and inflammation, raising the view that micronuclei play active roles in human aging and tumorigenesis. Thus, understanding the ways in which micronuclear envelope (mNE) goes awry acquires increased importance. Here, we review the data to present a general framework for this question. We firstly describe NE reassembly after mitosis and NE repair during interphase. Simultaneously, we briefly discuss how mNE is organized and how mNE rupture controls the fate of micronuclei and micronucleated cells. As a focus of this review, we highlight current knowledge about why mNE is rupture-prone and irreparable. For this, we survey observations from a series of elegant studies to provide a systematic overview. We conclude that the birth of rupture-prone and irreparable micronuclei may be the cumulative effects of their intracellular geographic origins, biophysical properties, and specific mNE features. We propose that DNA damage and immunogenicity in micronuclei increase stepwise from altered mNE components, mNE rupture, and refractory to repair. Throughout our discussion, we note interesting issues in mNE fragility that have yet to be resolved.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.