Chen H L, Chiu T S, Chen P J, Chen D S
Hepatitis Research Center, National Taiwan University Hospital, Taipei, Republic of China.
Cancer Genet Cytogenet. 1993 Feb;65(2):161-6. doi: 10.1016/0165-4608(93)90227-d.
Karyotyping of human liver cancer cell lines and chromosome in situ hybridization of hepatitis B virus (HBV) DNA was performed in order to elucidate the possible mechanism of hepatocarcinogenesis from evidence of chromosomal changes and HBV integration patterns. HepG2-2 and HepG2-5 cell lines were HepG2 cells experimentally transfected with HBV DNA; the HCC36 cell line was derived from a hepatocellular carcinoma containing integrated HBV DNA from a Taiwanese patient. HepG2 cells, a hepatoblastoma cell line without HBV DNA integration, served as negative control. In HepG2-2, HepG2-5, and HCC36 cells, multiple integrations of HBV DNA were observed by in situ hybridization and hybridization signals occurred preferentially on certain chromosomes: 2, 5, 10, 11, 18; 7, 10, 13, 17, 18; and 4, 6, 11, 12q+, 18; respectively. In addition, a strong correlation between chromosomal changes and HBV integration was noticed in HCC36 cells, especially at chromosome 12q+.
为了从染色体变化和乙肝病毒（HBV）整合模式的证据中阐明肝癌发生的可能机制，对人肝癌细胞系进行了核型分析，并对HBV DNA进行了染色体原位杂交。HepG2-2和HepG2-5细胞系是用HBV DNA实验转染的HepG2细胞；HCC36细胞系源自一名台湾患者的含有整合型HBV DNA的肝细胞癌。HepG2细胞是一种无HBV DNA整合的肝母细胞瘤细胞系，用作阴性对照。在HepG2-2、HepG2-5和HCC36细胞中，通过原位杂交观察到HBV DNA的多次整合，杂交信号优先出现在某些染色体上：分别为2、5、10、11、18号染色体；7、10、13、17、18号染色体；以及4、6、11、12q+、18号染色体。此外，在HCC36细胞中发现染色体变化与HBV整合之间存在很强的相关性，尤其是在12q+染色体上。
