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Recurrent chromosome alterations in hepatocellular carcinoma detected by comparative genomic hybridization

肝细胞癌 比较基因组杂交 肝硬化 生物 染色体 阶段(地层学) 基因 病理 胃肠病学 癌症研究 内科学 遗传学 医学 古生物学
作者
Xin Yuan Guan,Yan Fang,Jonathan S. T. Sham,Dora Lai Wan Kwong,Yaqi Zhang,Qiaoli Liang,Huimei Li,Huan‐Xiang Zhou,Jeffrey M. Trent
出处
期刊:Genes, Chromosomes and Cancer [Wiley]
卷期号:29 (2): 110-116 被引量:132
标识
DOI:10.1002/1098-2264(2000)9999:9999<::aid-gcc1022>3.0.co;2-v
摘要

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and has a very poor prognosis. Fifty primary HCC cases have been analyzed in the present study to explore the association between genomic alteration in primary HCC and clinical features. Several recurrent chromosomal abnormalities were identified in this study. The most frequently detected chromosomal gains involved chromosome arms 1q (33/50 cases, 66%), 8q (24/50 cases, 48%), and 20q (10/50 cases, 20%). High-copy-number amplifications involving 1q (4 cases), 8q (3 cases), and 20q (3 cases) were detected, and a minimum overlapping amplified region at 1q12–q22 was identified. The most frequently detected loss of chromosomal material involved 16q (35/50 cases, 70%), 17p (26/50 cases, 52%), 19p (21/50 cases, 42%), 4q (20/50 cases, 40%), 1p (18/50 cases, 36%), 8p (16/50 cases, 32%), and 22q (14/50 cases, 28%). The associations between genomic alterations detected in the present study and clinical features including clinical stage, tumor size, HBV infection, chronic liver disease, and liver cirrhosis were explored. Our CGH results suggest that the gain of 20q and deletion of 8p are late genetic alterations in HCC, because the incidence of these alterations was obviously increased in the advanced clinical stages. Another finding showed that loss of 8p and gain of 8q and 20q are associated with tumor size. The recurrent gain and loss of chromosomal regions identified in this study provide candidate regions that may contain oncogenes or tumor suppressor genes respectively involved in HCC development and progression. © 2000 Wiley-Liss, Inc.

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