간암종에서 9p, 13q, 16q 염색체의 Microsatellite 변이에 대한 연구

초록

Purpose: Hepatocellular carcinoma (HCC) patients are asymptomatic and the tumor remains in an unresectable state until the tumor progresses. Recently much efforts for elucidation of the early hepatocarcinogenesis have been made, and for this purpose it is very crucial to investigate the gengtic abnormalities. We evaluated microsatellite alterations of five markers form chromososme 9, 13, 16 and investigated the reiationships with the clinicopathoiogical parameters in HCC. Methods: The microsatellite alteration analysis was per formed using polymerase chain reaction with five polymorphic microsatellite markers (D9S171, D9S1747, A13S156, A16S419, D16S3106) in 40 surgically resected HCCs and their respective non-tumorous counterparts. Results: D9S171, D9S1747, A13S156, A16S419, D16S3106 abnrmalities were detected in 20.0%, 14.3%, 50.0%, 32.4% and 22.6%, respectively. Loss of heterozygosity (LOH) of D9S171 correlated well with higher tumor histologic grade and LOH of D13S156, D16S419 and D16S3106 correlated well with increased tumor size. Microsatellite instability (MSI) was found in two markers, D13S156, D16S419. Conclusion: As a result, we cincluded that alterations in microsatellites of various chromosomes may contribute to the hepatocarcinogenesis and tumor progression. Especially LOH of chromosome 13 and 16 are considered to correlate with tumor progression. (J Korean Surg Soc 2001;61:305-311)

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