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pubmed-article:17211475pubmed:abstractTextThe decatenation checkpoint delays entry into mitosis until the chromosomes have been disentangled. Deficiency in or bypass of the decatenation checkpoint can cause chromosome breakage and nondisjunction during mitosis, which results in aneuploidy and chromosome rearrangements in the daughter cells. A deficiency in the decatenation checkpoint has been reported in lung and bladder cancer cell lines and may contribute to the accumulation of chromosome aberrations that commonly occur during tumour progression. A checkpoint deficiency has also been documented in cultured stem and progenitor cells, and cancer stem cells are likely to be derived from stem and progenitor cells that lack an effective decatenation checkpoint. An inefficient decatenation checkpoint is likely to be a source of the chromosome aberrations that are common features of most tumours, but an inefficient decatenation checkpoint in cancer stem cells could also provide a potential target for chemotherapy.lld:pubmed
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pubmed-article:17211475pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:17211475pubmed:articleTitleThe decatenation checkpoint.lld:pubmed
pubmed-article:17211475pubmed:affiliationDepartment of Genetics and Development, College of Physicians and Surgeons of Columbia University, 701 W. 168th St., New York, NY 10032, USA.lld:pubmed
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