Journal
NATURE REVIEWS GENETICS
Volume 21, Issue 1, Pages 44-62Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41576-019-0171-x
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Funding
- European Molecular Biology Organization LongTerm Fellowship
- Human Frontier Science Program Postdoctoral Fellowship
- NIH [CA206157, GM118066]
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Cancer is driven by multiple types of genetic alterations, which range in size from point mutations to whole-chromosome gains and losses, known as aneuploidy. Chromosome instability, the process that gives rise to aneuploidy, can promote tumorigenesis by increasing genetic heterogeneity and promoting tumour evolution. However, much less is known about how aneuploidy itself contributes to tumour formation and progression. Unlike some pan-cancer oncogenes and tumour suppressor genes that drive transformation in virtually all cell types and cellular contexts, aneuploidy is not a universal promoter of tumorigenesis. Instead, recent studies suggest that aneuploidy is a context-dependent, cancer-type-specific oncogenic event that may have clinical relevance as a prognostic marker and as a potential therapeutic target.
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