Loss of heterozygosity of p53 in oral cancers demonstrated by the polymerase chain reaction

John S. Largey, Stephen J. Meltzer, Jing Yin, Kathleen Norris, John J. Sauk, David W. Archibald

Research output: Contribution to journalArticlepeer-review

Abstract

Background. Alterations in the tumor suppressor gene p53 are the most frequently detected genetic abnormalities in human cancers. Inactivated tumor suppressor genes, including p53, often are suggested by loss of heterozygosity (LOH) studies. p53 gene inactivation has been reported in esophageal cancers. Because the etiologic factors for esophageal and intraoral carcinomas often are the same, corresponding molecular events may occur in oral squamous cell carcinoma (SCC) development. Methods. The authors investigated LOH of the p53 gene in DNA from 27 primary oral cancers using a polymerase chain reaction (PCR)‐based restriction fragment length polymorphism assay. DNA from fixed specimens of SCC and normal tissues was isolated and amplified at two p53 gene polymorphic restriction sites. Results. In heterozygous individuals, 10 of 14 (71%) intraoral SCC demonstrated loss of p53 heterozygosity at one polymorphic restriction site. Two of five carcinomas showed LOH at a second site. Conclusions. These results suggest that inactivation of p53 is involved in the development or progression of SCC of the oral cavity.

Original languageEnglish (US)
Pages (from-to)1933-1937
Number of pages5
JournalCancer
Volume71
Issue number6
DOIs
StatePublished - Mar 15 1993
Externally publishedYes

Keywords

  • loss of heterozygosity
  • oral cancer
  • p53
  • tumor suppressor gene

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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