Piao Z, Park C, Park J H, Kim H
Department of Pathology, Yonsei University, College of Medicine, Seoul, Korea.
Int J Cancer. 1998 Jan 5;75(1):29-33. doi: 10.1002/(sici)1097-0215(19980105)75:1<29::aid-ijc5>3.0.co;2-3.
To elucidate the genetic events which may play important roles in hepatocarcinogenesis, we examined every non-acrocentric chromosome arm of 22 hepatocellular carcinomas (HCCs) for loss of heterozygosity (LOH) using 68 highly polymorphic microsatellite markers. Thirty-six (92%) of 39 chromosome arms showed LOH in at least one patient, however 3 chromosome arms, 2p, 2q, and 20q, did not show any LOH. High to moderate frequency of LOH (> 30% of informative cases) was observed at chromosomes 1q (68.1%), 4q (72.7%), 8p (63.6%), 8q (77.3%), 10q (33.3%), 13q (40%), 14q (46.1%), 16q (59.1%), and 17p (46.2%). Among these, LOH on chromosomes 1q and 8q have not been previously identified in HCC. Our results suggest that novel tumor suppressor genes may be involved in the development and progression of HCC.
为了阐明可能在肝癌发生过程中起重要作用的遗传事件，我们使用68个高度多态性微卫星标记，对22例肝细胞癌（HCC）的每条非近端着丝粒染色体臂进行杂合性缺失（LOH）检测。39条染色体臂中的36条（92%）在至少1例患者中显示出LOH，然而，2p、2q和20q这3条染色体臂未显示任何LOH。在1q（68.1%）、4q（72.7%）、8p（63.6%）、8q（77.3%）、10q（33.3%）、13q（40%）、14q（46.1%）、16q（59.1%）和17p（46.2%）染色体上观察到高至中等频率的LOH（>30%的信息性病例）。其中，1q和8q染色体上的LOH在HCC中此前尚未被发现。我们的结果表明，新的肿瘤抑制基因可能参与了HCC的发生和发展。
