ArticleCell division2010
Merotelic attachments and non-homologous end joining are the basis of chromosomal instability.
Article in Cell division, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Aneuploidy and complex genomic rearrangements in cancer evolution.Nature cancer · 2024Review
- Why not Y naught.Heredity · 2022Review
- Chromosomal instability upregulates interferon in acute myeloid leukemia.Genes, chromosomes & cancer · 2020Article
- Novel insight into the function of tankyrase.Oncology letters · 2018Review
- Chromosomal instability induced by increased BIRC5/Survivin levels affects tumorigenicity of glioma cells.BMC cancer · 2017Article
- Aurora kinase B dependent phosphorylation of 53BP1 is required for resolving merotelic kinetochore-microtubule attachment errors during mitosis.Oncotarget · 2017Article
- Achilles' heel of pluripotent stem cells: genetic, genomic and epigenetic variations during prolonged culture.Cellular and molecular life sciences : CMLS · 2016Review
- Multiple Small Supernumerary Marker Chromosomes Resulting from Maternal Meiosis I or II Errors.Molecular syndromology · 2016Article
- Survivin safeguards chromosome numbers and protects from aneuploidy independently from p53.Molecular cancer · 2014Article
- Chromothripsis: breakage-fusion-bridge over and over again.Cell cycle (Georgetown, Tex.) · 2013Article
- Let's huddle to prevent a muddle: centrosome declustering as an attractive anticancer strategy.Cell death and differentiation · 2012Review
- Linking stem cells to chromosomal instability.Oncoimmunology · 2012Article
- Ablation of Dido3 compromises lineage commitment of stem cells in vitro and during early embryonic development.Cell death and differentiation · 2012Article
- Centromere fission, not telomere erosion, triggers chromosomal instability in human carcinomas.Carcinogenesis · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the large majority of solid tumors show a combination of mitotic spindle defects and chromosomal instability, little is known about the mechanisms that govern the initial steps in tumorigenesis. The recent report of spindle-induced DNA damage provides evidence for a single mechanism responsible for the most prominent genetic defects in chromosomal instability. Spindle-induced DNA damage is brought about by uncorrected merotelic attachments, which cause kinetochore distortion, chromosome breakage at the centromere, and possible activation of DNA damage repair pathways. Although merotelic attachments are common early in mitosis, some escape detection by the kinetochore pathway. As a consequence, a proportion of merotelic attachments gives rise to chromosome breakage in normal cells and in carcinomas. An intrinsic chromosome segregation defect might thus form the basis of tumor initiation. We propose a hypothesis in which merotelic attachments and chromosome breakage establish a feedback loop that results in relaxation of the spindle checkpoint and suppression of anti-proliferative pathways, thereby promoting carcinogenesis.
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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.