J Korean Assoc Oral Maxillofac Surg.  2000 Aug;26(4):337-344.

MICROSATELLITE INSTABILITY AND p53 GENE MUTATION IN ORAL SQUAMOUS CELL CARCINOMA

• Choi TH
• Chung WB
• Hong SH
• Kim JA
• Na SO
• Jang HJ
• Sohn YK
• Kim CS
• Kim JW

Abstract

Germ-line mutations at DNA repair loci confer susceptibility to colon cancer in hereditary non-polypopsis colorectal cancer. Somatic loss of DNA mismatch repair gene has been reported in a large variety of other tumor types. Replication errors(RERs) judged by microsatellite instability(MSI) and its associated mutations have been recognized as an important mechanism in various tumor types. To investigate associations between MSI and oral squamous cell carcinoma, the frequency of MSI using 12 microsatellite markers were analyzed for the series of oral tumors. Of 17 tumors, 8 cases(47%) did not show instability at any of the 12 loci; 5(29%) showed instability at 2~3 loci; and 4(24%) showed instability above 4 loci. The 4 cases showing widespread MSI did not differ from those without evidence of instability in terms of age at diagnosis, degree of differentiation, metastasis to lymph node, tumor location or the presence of mutations in the p53 tumor suppressor gene. DCC and D17S 796 were the most frequently detected in MSI analysis. There were no correlation between smoking and MSI frequency, instead, smoking was suggested to increase the mutation rate of p53 and development of oral carcinomas.

Keyword

Microsatellite instability(MSI); Oral squamous cell carcinoma; p53

MeSH Terms

Carcinoma, Squamous Cell*
Colonic Neoplasms
Colorectal Neoplasms
Diagnosis
DNA Mismatch Repair
DNA Repair
Genes, p53*
Genes, Tumor Suppressor
Germ-Line Mutation
Lymph Nodes
Microsatellite Instability*
Microsatellite Repeats*
Mutation Rate
Neoplasm Metastasis
Smoke
Smoking
Smoke