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- W2013722663 abstract "High expression of Aurora-B has been observed in various cancers, and inhibition of this kinase has been shown to halt cellular proliferation. However, the mechanism of effect of Aurora-B on cellular transformation has not been fully explored. Here, we show that overexpression of Aurora-B in murine epithelial cells promotes generation of tetraploids. In search of a related mechanism, spectral karyotyping was carried out, showing premature chromatid separation (PCS). Of interest, PCS is a hallmark of Robert's syndrome, which also involves cellular polyploidy and aneu- ploidy. Sorted tetraploid Aurora-B-overexpressing cells promoted significant mammary epithelial cancers when injected into nude mice, as compared to injection of nonfractionated cells, suggesting that tetraploidy is an important mediator of Aurora-B-induced tumorigenesis. Comparative chromosome hybridization performed on DNA derived from tetraploid cell-induced tumors indicates amplifications and deletions of regions throughout the genome, which include tumor-promoting or tumorsuppressing genes, respectively. Thus, sustained expression of Aurora-B induces tetraploidy, which, in turn, facilitates genomic instability and tumor development in a xenograft model.— Nguyen, H. G., Makitalo, M., Yang, D., Chinnappan, D., St. Hilaire, C., Ravid, K. Deregulated Aurora-B induced tetraploidy promotes tumorigenesis. FASEBJ. 23, 2741–2748 (2009)" @default.
- W2013722663 created "2016-06-24" @default.
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- W2013722663 date "2009-03-30" @default.
- W2013722663 modified "2023-10-16" @default.
- W2013722663 title "Deregulated Aurora‐B induced tetraploidy promotes tumorigenesis" @default.
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- W2013722663 doi "https://doi.org/10.1096/fj.09-130963" @default.
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