Loss of heterozygosity of p53 in oral cancers demonstrated by the polymerase chain reaction
| Autor: | Kathleen Norris, Jing Yin, David W. Archibald, John J. Sauk, Stephen J. Meltzer, John S. Largey |
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| Rok vydání: | 1993 |
| Předmět: |
Cancer Research
Tumor suppressor gene Biology Molecular biology law.invention Loss of heterozygosity stomatognathic diseases Restriction site chemistry.chemical_compound Oncology chemistry law Gene expression Cancer research Restriction fragment length polymorphism Gene Polymerase chain reaction DNA |
| Zdroj: | Cancer. 71:1933-1937 |
| ISSN: | 1097-0142 0008-543X |
| DOI: | 10.1002/1097-0142(19930315)71:6<1933::aid-cncr2820710602>3.0.co;2-d |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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