MICROSATELLITE INSTABILITY AND p53 GENE MUTATION IN ORAL SQUAMOUS CELL CARCINOMA.
- Author:
Tae Ho CHOI
1
;
Woon Bok CHUNG
;
Su Hyung HONG
;
Jin A KIM
;
Sun oung NA
;
Hyun Jung JANG
;
Yoon Kyung SOHN
;
Chin Soo KIM
;
Jung Wan KIM
Author Information
1. Department of Oral and Maxillofacial Surgery, College of Medicine, Kyungpook National University, Taegu,Korea.
- Publication Type:Original Article
- Keywords:
Microsatellite instability(MSI);
Oral squamous cell carcinoma;
p53
- MeSH:
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
- From:Journal of the Korean Association of Oral and Maxillofacial Surgeons
2000;26(4):337-344
- CountryRepublic of Korea
- Language:Korean
-
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.
