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구강편평상피세포암 조직에서의 Microsatellite 불안정성 및 p53 유전자 돌연변이 분석
최태호(Tae Ho Choi),정운복(Woon Bok Chung),홍수형(Su Hyung Hong),김진아(Jin A Kim),나선영(Sun oung Na),장현중(Hyun Jung Jang),손윤경(Yoon Kyung Sohn),김진수(Chin Soo Kim),김정완(Jung Wan Kim) 대한구강악안면외과학회 2000 대한구강악안면외과학회지 Vol.26 No.4
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.