ReviewCarcinogenesis2011
Centromere fission, not telomere erosion, triggers chromosomal instability in human carcinomas.
Review in Carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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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.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- HOROSCOPE: Decoding human centromere architecture from short reads usingbioRxiv : the preprint server for biology · 2026Article
- Higher order repeat structures reflect diverging evolutionary paths in maize centromeres and knobs.Genome biology · 2026Article
- Sex-specific DNA-replication in the early mammalian embryo.Nature communications · 2024Article
- Flexible Attachment and Detachment of Centromeres and Telomeres to and from Chromosomes.Biomolecules · 2023Review
- ERCC6L2 mitigates replication stress and promotes centromere stability.Cell reports · 2023Article
- Breaking the paradigm: early insights from mammalian DNA breakomes.The FEBS journal · 2022Review
- Article
- BRCA1 prevents R-loop-associated centromeric instability.Cell death & disease · 2021Article
- Molecular Complexes at Euchromatin, Heterochromatin and Centromeric Chromatin.International journal of molecular sciences · 2021Review
- Article
- Heterochromatin suppresses gross chromosomal rearrangements at centromeres by repressing Tfs1/TFIIS-dependent transcription.Communications biology · 2019Article
- Repetitive Fragile Sites: Centromere Satellite DNA As a Source of Genome Instability in Human Diseases.Genes · 2018Review
- The dark side of centromeres: types, causes and consequences of structural abnormalities implicating centromeric DNA.Nature communications · 2018Review
- Article
- DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.Stem cell reports · 2017Article
- Review
- Review
- Replication, checkpoint suppression and structure of centromeric DNA.Nucleus (Austin, Tex.) · 2016Review
- Aberrant reduction of telomere repetitive sequences in plasma cell-free DNA for early breast cancer detection.Oncotarget · 2015Article
- Replication stress in early S phase generates apparent micronuclei and chromosome rearrangement in fission yeast.Molecular biology of the cell · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of sporadic carcinomas suffer from a kind of genetic instability in which chromosome number changes occur together with segmental defects. This means that changes involving intact chromosomes accompany breakage-induced alterations. Whereas the causes of aneuploidy are described in detail, the origins of chromosome breakage in sporadic carcinomas remain disputed. The three main pathways of chromosomal instability (CIN) proposed until now (random breakage, telomere fusion and centromere fission) are largely based on animal models and in vitro experiments, and recent studies revealed several discrepancies between animal models and human cancer. Here, we discuss how the experimental systems translate to human carcinomas and compare the theoretical breakage products to data from patient material and cancer cell lines. The majority of chromosomal defects in human carcinomas comprises pericentromeric breaks that are captured by healthy telomeres, and only a minor proportion of chromosome fusions can be attributed to telomere erosion or random breakage. Centromere fission, not telomere erosion, is therefore the most probably trigger of CIN and early carcinogenesis. Similar centromere-telomere fusions might drive a subset of congenital defects and evolutionary chromosome changes.
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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.