Liu J, Li H, Nomura K, Ohtake K, Kitagawa T
Department of Pathology, Japanese Foundation for Cancer Research, Tokyo.
J Cancer Res Clin Oncol. 1992;118(8):601-5. doi: 10.1007/BF01211804.
In order to shed light on the causal mechanisms of hepatocarcinogenesis in the transgenic mouse into which the albumin-promotor-regulated SV40-T antigen gene has been introduced (T+ mouse), and especially on the frequent chromosomal aberrations seen in cultured hepatocytes and hepatocellular neoplasms derived from such animals, the frequency of sister chromatid exchange (SCE) and karyotype abnormalities were investigated in a hepatocyte primary culture system. Cells were obtained through collagenase perfusion from T+ mice at 16-18 days of age, when no morphological changes are apparent, and from nontransgenic littermates, and cultured in the presence of bromodeoxyuridine. SCE was seen in transgenic hepatocytes twice as frequently as in their normal counterparts. No karyotype abnormalities in terms of numerical change or gross aberration were detected at this phase. The results thus suggest mutagenic properties for the T antigen, which may play an important role in hepatocarcinogenesis in this transgenic mouse.
为了阐明在已导入白蛋白启动子调控的SV40-T抗原基因的转基因小鼠（T+小鼠）中肝癌发生的因果机制，尤其是在源自此类动物的培养肝细胞和肝细胞肿瘤中常见的染色体畸变，在肝细胞原代培养系统中研究了姐妹染色单体交换（SCE）频率和核型异常情况。通过胶原酶灌注从16 - 18日龄（此时无明显形态学变化）的T+小鼠及其非转基因同窝小鼠获取细胞，并在溴脱氧尿苷存在的情况下进行培养。转基因肝细胞中观察到的SCE频率是其正常对应细胞的两倍。在此阶段未检测到数量变化或明显畸变方面的核型异常。因此，结果表明T抗原具有诱变特性，这可能在这种转基因小鼠的肝癌发生中起重要作用。
