Accumulating mutations of p53 in colon tumor and hairy cell leukemia do not arise from methylation/deamination processes, but rather from nucleotide deletions and insertions

Biol Chem. 1998 Apr-May;379(4-5):545-7.

Abstract

Mutations of the p53 gene may alter the specific regulatory domains of the protein. We examined the conserved domains III, IV and V by SSCP using PCR primers covering exons 5, 6, 7 and 8 from hairy cell leukemia (HCL), polyps, colorectal and gastric carcinomas. A low rate of p53 mutations was detected in HCL and polyps. These mutations may predict the risk of malignant development. However, multiple mutations were a frequent occurrence in tumors. Sequence analysis of our samples did not demonstrate the high frequency of transition mutations (C-->T) that would be predicted if the major course of p53 mutations is deamination of 5-methylcytosine (5mC). Rather, most mutations were found to be single base insertions or deletions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Colonic Polyps / genetics*
  • Colonic Polyps / pathology
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / pathology
  • DNA Methylation*
  • Deamination
  • Genes, p53*
  • Humans
  • Leukemia, Hairy Cell / genetics*
  • Leukemia, Hairy Cell / pathology
  • Mutagenesis, Insertional
  • Mutation*
  • Polymerase Chain Reaction
  • Polymorphism, Single-Stranded Conformational
  • Sequence Deletion
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / pathology