Zhu M H
Department of Pathology, Fourth Military Medical University, Xi'an.
Zhonghua Zhong Liu Za Zhi. 1993 Jul;15(4):245-7.
Fourty-five cases of primary hepatocellular carcinoma (PHC) from areas of low aflatoxin B1 exposure but high risk of hepatitis B (HBV) were examined. Positive cases of HBV-DNA were determined in 40 of 45 cases by southern hybridization and polymerase chain reaction (PCR). Results of restriction fragment length polymorphism (RFLP) analysis showed that 1 of 33 informative cases revealed loss of heterozygosity at p53 gene locus. The point mutation of p53 exon 7 was detected by PCR and restriction enzyme digestion with RsaI, MspI and HaeIII, respectively. Only two of the 45 cases showed point mutation on codon 247 and 249, and sequence analysis showed that the changes were C-->G and G-->T, respectively. Frozen section examinations in 1 of 5 cases showed weak positive staining on nucleus by immunohistochemistry with anti-p53 monoclonal antibody (pAb1801). Our results provide evidence suggesting that HBV infection alone do not contribute to changes of p53 gene including allelic loss and point mutation. A multiple step process may exist and multiple genes may be involved in hepatocarcinogenesis.
对来自黄曲霉毒素B1暴露水平低但乙肝（HBV）感染风险高的地区的45例原发性肝细胞癌（PHC）病例进行了检查。通过Southern杂交和聚合酶链反应（PCR）在45例中的40例中检测到HBV-DNA阳性病例。限制性片段长度多态性（RFLP）分析结果显示，33例信息丰富的病例中有1例在p53基因位点显示杂合性缺失。分别通过PCR以及用RsaI、MspI和HaeIII进行限制性酶切检测p53第7外显子的点突变。45例病例中只有2例在密码子247和249处显示点突变，序列分析表明变化分别为C→G和G→T。5例中的1例冰冻切片检查显示，用抗p53单克隆抗体（pAb1801）进行免疫组织化学检测时细胞核呈弱阳性染色。我们的结果提供了证据，表明单独的HBV感染不会导致p53基因的改变，包括等位基因缺失和点突变。可能存在一个多步骤过程，并且多个基因可能参与肝癌发生。
