Lau Sze-hang, Guan Xin-yuan
Department of Clinical Oncology, Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Acta Pharmacol Sin. 2005 Jun;26(6):659-65. doi: 10.1111/j.1745-7254.2005.00126.x.
Specific chromosome aberrations are frequently detected during the development of hepatocellular carcinoma. Molecular cytogenetic approaches such as comparative genomic hybridization and loss of heterozygosity analyses have provided fruitful information on changes in HCC cases at the genomic level. Mapping of chromosome gains and losses have frequently resulted in the identification of oncogenes and tumor suppressors, respectively. In this review, we summarize some frequently detected chromosomal aberrations reported for hepatocellular carcinoma cases using comparative genomic hybridization and loss of heterozygosity studies. Focus will be on gains of 1q, 8q, and 20q, and losses of 4q, 8p, 13q, 16q, and 17p. We then examine the candidate oncogenes and tumor suppressors located within these regions, and explore their possible functions in hepatocarcinogenesis. Finally, the impact of microarray-based screening platforms will be discussed.
在肝细胞癌发生发展过程中常可检测到特定的染色体畸变。诸如比较基因组杂交和杂合性缺失分析等分子细胞遗传学方法，已在基因组水平上为肝细胞癌病例的变化提供了丰富信息。染色体增减图谱常常分别导致癌基因和肿瘤抑制基因的鉴定。在本综述中，我们总结了利用比较基因组杂交和杂合性缺失研究报道的肝细胞癌病例中一些常检测到的染色体畸变。重点将放在1q、8q和20q的增加，以及4q、8p、13q、16q和17p的缺失上。然后，我们研究位于这些区域内的候选癌基因和肿瘤抑制基因，并探讨它们在肝癌发生中的可能作用。最后，将讨论基于微阵列的筛查平台的影响。
