Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis

Andrew J. Holland; Don W. Cleveland

doi:10.1038/nrm2718

Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis

Research output: Contribution to journal › Review article › peer-review

Abstract

The mitotic checkpoint is a major cell cycle control mechanism that guards against chromosome missegregation and the subsequent production of aneuploid daughter cells. Most cancer cells are aneuploid and frequently missegregate chromosomes during mitosis. Indeed, aneuploidy is a common characteristic of tumours, and, for over 100 years, it has been proposed to drive tumour progression. However, recent evidence has revealed that although aneuploidy can increase the potential for cellular transformation, it also acts to antagonize tumorigenesis in certain genetic contexts. A clearer understanding of the tumour suppressive function of aneuploidy might reveal new avenues for anticancer therapy.

Original language	English (US)
Pages (from-to)	478-487
Number of pages	10
Journal	Nature Reviews Molecular Cell Biology
Volume	10
Issue number	7
DOIs	https://doi.org/10.1038/nrm2718
State	Published - Jul 2009
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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10.1038/nrm2718

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title = "Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis",

abstract = "The mitotic checkpoint is a major cell cycle control mechanism that guards against chromosome missegregation and the subsequent production of aneuploid daughter cells. Most cancer cells are aneuploid and frequently missegregate chromosomes during mitosis. Indeed, aneuploidy is a common characteristic of tumours, and, for over 100 years, it has been proposed to drive tumour progression. However, recent evidence has revealed that although aneuploidy can increase the potential for cellular transformation, it also acts to antagonize tumorigenesis in certain genetic contexts. A clearer understanding of the tumour suppressive function of aneuploidy might reveal new avenues for anticancer therapy.",

author = "Holland, {Andrew J.} and Cleveland, {Don W.}",

note = "Funding Information: The authors thank W. Silkworth, D. Cimini, N. Ganem and D. Pellman for sharing results before publication. We apologize to all those whose work could not be cited owing to space limitations. D.W.C. receives salary support from the Ludwig Institute for Cancer Research and A.J.H. is supported by a European Molecular Biology Organization (EMBO) Long-Term Fellowship.",

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PY - 2009/7

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N2 - The mitotic checkpoint is a major cell cycle control mechanism that guards against chromosome missegregation and the subsequent production of aneuploid daughter cells. Most cancer cells are aneuploid and frequently missegregate chromosomes during mitosis. Indeed, aneuploidy is a common characteristic of tumours, and, for over 100 years, it has been proposed to drive tumour progression. However, recent evidence has revealed that although aneuploidy can increase the potential for cellular transformation, it also acts to antagonize tumorigenesis in certain genetic contexts. A clearer understanding of the tumour suppressive function of aneuploidy might reveal new avenues for anticancer therapy.

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Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis

Abstract

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