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为了解在黄曲霉毒素Ｂ１（ＡＦＢ１）低含量区以ＨＢＶ为主要危险因素的ＨＣＣｐ５３基因突变情况，并分析它与ＨＢＶ及其它因素的关系，作者筛检了成都地区３２例原发性肝癌（ＨＣＣ），分别应用ＰＣＲ－ＲＦＬＰＳｏｕｔｈｅｒｎ吸印杂交及免疫组化染色法检测了３２例ＨＣＣ及２７份癌旁肝组织中ｐ５３基因突变、ＨＢＶＤＮＡ整合及ＨＢｓＡｇ表达。结果：所有ＨＣＣ病例均感染过ＨＢＶ，肝癌细胞中ＨＢＶＤＮＡ整合率７１．９％，癌旁组织均有肝硬化或／和慢活肝病变，且ＨＢｓＡｇ表达率９６．３％。３２例ＨＣＣ中检出８例Ｐ５３蛋白阳性（２５％），这种改变与ＨＢＶＤＮＡ整合及ＨＢｓＡｇ表达无明显关系，而与ＨＣＣ发生年龄有关；３２例ＨＣＣ组织中有２例ｐ５３基因第２４９号编码子突变（６．２５％），明显低于ＡＦＢ１高含量区ＨＣＣ，而与台湾、日本等ＡＦＢ１低含量区报道一致，提示：成都地区ＨＣＣ与ＨＢＶ感染确有密切关系；ｐ５３改变在ＨＣＣ发生上有一定作用，但是多数ＨＣＣ并无ｐ５３基因突变又提示ＨＣＣ发生尚涉及其它复杂机制；ＨＢＶ在ＨＣＣｐ５３基因改变中的作用机制值得进一步探索。
To understand the relationship between HCC p53 gene mutation and HBV and other factors in the low-content area of aflatoxin B1 (AFB1) with HBV as the main risk factor, the authors screened 32 cases of primary liver cancer (HCC) in Chengdu. The p53 gene mutation, HBV DNA integration, and HBsAg expression were detected in 32 HCC and 27 adjacent liver tissues by PCR-RFLP Southern blot hybridization and immunohistochemical staining, respectively. RESULTS: All HCC cases were infected with HBV. The rate of HBV DNA integration in hepatoma cells was 71.9%. Pericarcinoma tissues had cirrhosis or chronic liver disease, and the HBsAg expression rate was 96.3%. 8 cases of P53 protein were detected in 32 cases of HCC (25%). This change was not related to the integration of HBV DNA and HBsAg expression, but related to the age of HCC; there were 2 cases of p53 gene No. 249 in 32 cases of HCC tissues. The sub-mutation (6.25%) was significantly lower than that of AFB1 with high content of HCC, which was consistent with the report of low-content areas of AFB1 in Taiwan, Japan, etc. It is suggested that HCC in Chengdu is closely related to HBV infection; p53 changes in HCC There is a certain role, but there is no p53 gene mutation in most HCCs and it suggests that there are other complicated mechanisms involved in HCC. The mechanism of HBV in HCCp53 gene alterations deserves further exploration.