The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Mad2-induced chromosome instability leads to lung tumour relapse after oncogene withdrawal
Open accessAbstract
Inhibition of an initiating oncogene often leads to extensive tumour cell death, a phenomenon known as oncogene addiction. This has led to the search for compounds that specifically target and inhibit oncogenes as anticancer agents. However, there has been no systematic exploration of whether chromosomal instability generated as a result of deregulation of the mitotic checkpoint pathway, a frequent characteristic of solid tumours, has any effect on oncogene addiction. Here we show that induction of chromosome instability by overexpression of the mitotic checkpoint gene Mad2 in mice does not affect the regression of Kras-driven lung tumours when Kras is inhibited. However, tumours that experience transient Mad2 overexpression and consequent chromosome instability recur at markedly elevated rates. The recurrent tumours are highly aneuploid and have varied activation of pro-proliferative pathways. Thus, early chromosomal instability may be responsible for tumour relapse after seemingly effective anticancer treatments.
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Self-citationDeterminants and clinical implications of chromosomal instability in cancer
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Metadata
- Authors
- Sotillo, R., Schvartzman, J.-M., Socci, N. D., & Benezra, R.
- Venue
- Nature
- Published
- 2010-02-21
- Volume
- 464
- Issue
- 7287
- Pages
- 436-440
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1987369248
- Cited by
- 273
- References
- 28
- FWCI
- 9.62
- Type
- journal article
- Language
- en
- Open access
- green
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