Abstract：
:Loss of cell cycle control and acquisition of chromosomal rearrangements such as gene amplification often occur during tumor progression, suggesting that they may be correlated. We show here that the wild-type p53 allele is lost when fibroblasts from patients with the Li-Fraumeni syndrome (LFS) are passaged in vitro. Normal and LFS cells containing wild-type p53 arrested in G1 when challenged with the uridine biosynthesis inhibitor PALA and did not undergo PALA-selected gene amplification. The converse occurred in cells lacking wild-type p53 expression. Expression of wild-type p53 in transformants of immortal and tumor cells containing mutant p53 alleles restored G1 control and reduced the frequency of gene amplification to undetectable levels. These studies reveal that p53 contributes to a metabolically regulated G1 check-point, and they provide a model for understanding how abnormal cell cycle progression leads to the genetic rearrangements involved in tumor progression.
journal_name
Celljournal_title
Cellauthors
Yin Y,Tainsky MA,Bischoff FZ,Strong LC,Wahl GMdoi
10.1016/0092-8674(92)90244-7subject
Has Abstractpub_date
1992-09-18 00:00:00pages
937-48issue
6eissn
0092-8674issn
1097-4172pii
0092-8674(92)90244-7journal_volume
70pub_type
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