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Bunz, F.* ; Fauth, C.* ; Speicher, M.R.* ; Dutriaux, A.* ; Sedivy, J.M.* ; Kinzler, K.W.* ; Vogelstein, B.* ; Lengauer, C.*

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

Cancer Res. 62, 1129-1133 (2002)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2002
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0008-5472
e-ISSN 1538-7445
Zeitschrift Cancer Research
Quellenangaben Band: 62, Heft: 4, Seiten: 1129-1133 Artikelnummer: , Supplement: ,
Verlag American Association for Cancer Research (AACR)
Verlagsort Philadelphia, Pa.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Human Genetics (IHG)
PubMed ID 11861393
Erfassungsdatum 2002-12-31
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