Targeted inactivation of p53 in human cells does not result in aneuploidy

Fred Bunz, Kenneth W. Kinzler, Bert Vogelstein, Christoph Lengauer, Christine Fauth, Michael R. Speicher, Annie Dutriaux, John M. Sedivy

Research output: Contribution to journalArticlepeer-review

160 Scopus citations


Because p53 mutation and aneuploidy usually coexist, it has been suggested that p53 inactivation leads to aneuploidy. We have rigorously tested this hypothesis in diploid human cell lines in which p53 was experimentally inactivated by targeted homologous recombination. Cells completely deficient in p53 did not become aneuploid, although a slight tendency toward tetraploidization was observed. No increased rates of numerical or structural chromosomal instabilities were observed in the p53-deficient cells. Rates of sister chromatid exchange and homologous recombination were also unaffected by p53 status. These results show that inactivation of p53 does not, in and of itself, lead to the development of aneuploidy.

Original languageEnglish (US)
Pages (from-to)1129-1133
Number of pages5
JournalCancer Research
Issue number4
StatePublished - Feb 15 2002

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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