Cited by 668Microtubule and mitosis dynamicsChromosomal and Genetic VariationsCancer-related Molecular Pathways

Tetraploidy, aneuploidy and cancer

Ganem, Neil J, Storchova, Zuzana, Pellman, David·2007·Current Opinion in Genetics & Development

Abstract

Aneuploidy is one of the most obvious differences between normal and cancer cells. However, there remains debate over how aneuploid cells arise and whether or not they are a cause or consequence of tumorigenesis. One proposed route to aneuploid cancer cells is through an unstable tetraploid intermediate. Supporting this idea, recent studies demonstrate that tetraploidy promotes chromosomal aberrations and tumorigenesis in vivo. These tetraploid cells can arise by a variety of mechanisms, including mitotic slippage, cytokinesis failure, and viral-induced cell fusion. Furthermore, new studies suggest that there might not be a ploidy-sensing checkpoint that permanently blocks the proliferation of tetraploid cells. Therefore, abnormal division of tetraploid cells might facilitate genetic changes that lead to aneuploid cancers.

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Crossref · 10.1016/j.gde.2007.02.011

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  • Polyploidy is considered a prerequisite to aneuploidy.

    “Polyploidy is considered a prerequisite to aneuploidy (Fujiwara et al., 2005, Ganem et al., 2007, Storchova and Kuffer, 2008, Thompson et al., 2010, Vitale et al., 2010)”
  • The polyploidy observed in Mdm2 transgenic cells is likely due at least in part to inhibition of p53 by Mdm2.

    “Since Mdm2 negatively regulates p53 (Marine and Lozano, 2010), and p53 inhibits the development of tetraploidy (Fujiwara et al., 2005, Ganem et al., 2007, Storchova and Kuffer, 2008, Thompson et al., 2010, Vitale et al., 2010), the polyploidy we observed in Mdm2 transgenic cells is likely due at least in part to inhibition of p53 by Mdm2.”

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Authors
Ganem, N. J., Storchova, Z., & Pellman, D.
Affiliations
  • Harvard University (US)
  • Boston Children's Hospital (US)
Corresponding author
Pellman, David
Venue
Current Opinion in Genetics & Development
Publisher
Elsevier BV
Published
2007-04
Volume
17
Issue
2
Pages
157-162
ISSN
0959-437X (ISSN-L)
OpenAlex
W2045802318
Cited by
668
References
52
Citations by year
2026: 13 · 2025: 10 · 2024: 18 · 2023: 17 · 2022: 18 · 2021: 22 · 2020: 31 · 2019: 39 · 2018: 46 · 2017: 34 · 2016: 38 · 2015: 50 · 2014: 29 · 2013: 43 · 2012: 57
FWCI
3.59
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Genetics & Development (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ca098537-09)
  • National Cancer Institute (R01CA98537)
  • National Institute of General Medical Sciences (T32GM008704)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords
tetraploidy, aneuploidy, cancer, carcinogenesis, chromosomal instability, mitotic slippage, cytokinesis failure, polyploidy
MeSH terms
Aneuploidy, DNA Replication, Humans, Models, Genetic, Neoplasms, Polyploidy, Tumor Suppressor Protein p53, Genomic Instability, Cell Proliferation

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