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Genomic Instability and Apoptosis Are Frequent in P53 Deficient Young Mice

  1. Author:
    Fukasawa, K.
    Wiener, F.
    Vande Woude, G. F.
    Mai

  2. Author Address

    Mai SB MANITOBA CANC TREATMENT & RES FDN MANITOBA INST CELL BIOL 100 OLIVIA ST WINNIPEG MB R3E 0V9 CANADA MANITOBA CANC TREATMENT & RES FDN MANITOBA INST CELL BIOL WINNIPEG MB R3E 0V9 CANADA UNIV MANITOBA DEPT PHYSIOL WINNIPEG MB R3E 0V9 CANADA NCI FREDERICK CANC RES & DEV CTR ABL BASIC RES PROGRAM FREDERICK, MD 21702 USA UNIV CINCINNATI COLL MED DEPT CELL BIOL NEUROBIOL & ANAT CINCINNATI, OH USA KAROLINSKA INST CTR MICROBIOL & TUMOR BIOL S-17177 STOCKHOLM SWEDEN
    1. Year: 1997
  2. Journal: Oncogene
    1. 15
    2. 11
    3. Pages: 1295-1302
  4. Type of Article: Article
  1. Abstract:

    The loss of p53 tumor suppressor functions results in genetic instability, characteristically associated with changes in chromosome ploidy and gene amplification. In vivo, we find that cells from various organs of 4 to 6-week old p53-nullizygous (p53 (-/-)) mice display aneuploidy and frequent gene amplification as well as evidence for apoptosis. Regardless of tissue types, many p53 (-/-) cells contain multiple centrosomes and abnormally formed mitotic spindles. Thus, chromosome vivo may be associated with abnormal Moreover, we observed a significant increase in the number of cells overexpressing c-Myc in p53 (-/-) mice. Consistent with previous studies showing that c-Myc overexpression is associated with gene amplification in vitro, many of the p53 (-/-) cells exhibited, in the same cell, c-Myc overexpression and amplified c-myc, dihydrofolate reductase (DHFR), and carbamoyl-phosphate synthetase-aspartate transcarbamoyl-dihydroorotase (CAD) genes. Furthermore, apoptosis was frequently observed in cells isolated from p53 (-/-) mice. The apoptotic cells contained abnormally amplified centrosomes, displayed aneuploidy, high levels of c-Myc expression, as web as gene amplification. These results indicate that a high number of aberrant cells is eliminated by p53-independent pathways in vivo. [References: 49]

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