Abstract
We analyzed all published deletions and insertions in the p53 gene to assess the relevance of mutagenesis models. Almost all deletions and insertions can be explained by one or more of the following DNA sequence features: monotonic base runs, adjacent or nonadjacent repeats of short tandem sequences, palindromes, and runs of purines or pyrimidines (homocopolymer runs). Increased length of monotonic runs correlates positively with increased frequency of events. Complex frameshift mutations can be explained by the formation of quasi-palindromes, with mismatch excision and replication using one strand of the palindrome as a template. Deletions and insertions in the p53 tumor suppressor gene may reflect both spontaneous and carcinogen-induced mutagenesis.
Footnotes
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↵1 To whom requests for reprints should be addressed, at Laboratory of Human Carcinogeneis, National Cancer Institute, National Institutes of Health, Building 37, Room 2C05, Bethesda, MD 20892-4255. Phone: (301) 496-2048; Fax: (301) 496-0497.
- Received September 11, 1995.
- Accepted March 4, 1996.
- ©1996 American Association for Cancer Research.
Volume 56, Issue 9
