ArticleProceedings of the National Academy of Sciences of the United States of America2013
Whole chromosome gain does not in itself confer cancer-like chromosomal instability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Cumulative disruption of regulatory genes precedes whole-chromosome gains in acute myeloid leukemia.Leukemia · 2026Article
- Disentangling the roles of aneuploidy, chromosomal instability and tumour heterogeneity in developing resistance to cancer therapies.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- Clonal origin and development of high hyperdiploidy in childhood acute lymphoblastic leukaemia.Nature communications · 2023Article
- Consequences of chromosome gain: A new view on trisomy syndromes.American journal of human genetics · 2022Review
- Review
- Aneuploidy: Cancer strength or vulnerability?International journal of cancer · 2019Review
- Non-random Mis-segregation of Human Chromosomes.Cell reports · 2018Article
- The impact of mitotic errors on cell proliferation and tumorigenesis.Genes & development · 2018Review
- Cellular Stress Associated with Aneuploidy.Developmental cell · 2018Review
- Understanding aneuploidy in cancer through the lens of system inheritance, fuzzy inheritance and emergence of new genome systems.Molecular cytogenetics · 2018Review
- Co-culture with lung cancer A549 cells promotes the proliferation and migration of mesenchymal stem cells derived from bone marrow.Experimental and therapeutic medicine · 2017Article
- Living in CIN: Mitotic Infidelity and Its Consequences for Tumor Promotion and Suppression.Developmental cell · 2016Review
- The fetal thymus has a unique genomic copy number profile resulting from physiological T cell receptor gene rearrangement.Scientific reports · 2016Article
- Article
- Aneuploidy and chromosomal instability in cancer: a jackpot to chaos.Cell division · 2015Article
- Does aneuploidy destabilize karyotypes automatically?Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Reply to Duesberg: Stability of peritriploid and triploid states in neoplastic and nonneoplastic cells.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Reply to Heng: Inborn aneuploidy and chromosomal instability.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Distinguishing constitutional and acquired nonclonal aneuploidy.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutional aneuploidy is typically caused by a single-event meiotic or early mitotic error. In contrast, somatic aneuploidy, found mainly in neoplastic tissue, is attributed to continuous chromosomal instability. More debated as a cause of aneuploidy is aneuploidy itself; that is, whether aneuploidy per se causes chromosomal instability, for example, in patients with inborn aneuploidy. We have addressed this issue by quantifying the level of somatic mosaicism, a proxy marker of chromosomal instability, in patients with constitutional aneuploidy by precise background-filtered dual-color FISH. In contrast to previous studies that used less precise methods, we find that constitutional trisomy, even for large chromosomes that are often trisomic in cancer, does not confer a significantly elevated rate of somatic chromosomal mosaicism in individual cases. Constitutional triploidy was associated with an increased level of somatic mosaicism, but this consisted mostly of reversion from trisomy to disomy and did not correspond to a proportionally elevated level of chromosome mis-segregation in triploids, indicating that the observed mosaicism resulted from a specific accumulation of cells with a hypotriploid chromosome number. In no case did the rate of somatic mosaicism in constitutional aneuploidy exceed that of "chromosomally stable" cancer cells. Our findings show that even though constitutional aneuploidy was in some cases associated with low-level somatic mosaicism, it was insufficient to generate the cancer-like levels expected if aneuploidy single-handedly triggered cancer-like chromosomal instability.
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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.