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目的分析和探讨ｐ５３异常对人肝细胞癌（ＨＣＣ）术后复发与生存的影响，以及其在ＨＣＣ发生发展中的作用机制．方法手术切除ＨＣＣ标本２０２例．分别来自启东ＨＣＣ高发区和上海等一般地区，其中行二次或多次手术患者５４例，组织学检测ＨＢｓＡｇ阳性患者１３８例（６８３％），ＨＢＶＤＮＡ原位杂交检测阳性患者８６例（４２６％），采用ＰＣＲＳＳＣＰ和ＲＦＣＰ技术结合免疫组化示综显示，分析ｐ５３基因５，６，７，８外显子突变及其编码蛋白的过度表达．结果ｐ５３基因突变率为４４６％（３３／７４），其中８９８％（２７／７３）表现为点突变，１８２％（６／３３）为片段性碱基缺失，长度１０ｂｐ～１６ｂｐ．等位基因杂合性缺失（ＬＯＨ）主要集中于外显子７和８，各与３９４％（１３／３３）和２７３％（９／３３）．外显子５和６的突变发生率各为１８２％（６／３３）和１５１％（５／３３）．外显子７ＲＦＬＰ分析证实第２４９位密码子有颠换突变（５３８％，７／１３）外，２４８位密码子也有点突变发生（３０８％，４／１３）．免疫组化检测显示Ｐ５３蛋白过度表达的总检出率为７０３％（１４２／２０２），ｐＡｂ１８０１与ＣＭ１ｍＡｂ检测Ｐ５３蛋白?
Objective To analyze and investigate the effect of p53 abnormality on recurrence and survival of human hepatocellular carcinoma (HCC) and its mechanism in the development of HCC. Methods Totally 202 cases of HCC were resected. 54 cases were diagnosed as HBsAg-positive patients by histology, 86 cases were positive by HBVDNA in situ hybridization (42 cases) 6%), using PCR SSCP and RFCP technology combined with immunohistochemistry showed comprehensive analysis of p53 gene 5,6,7,8 exon mutation and its encoded protein overexpression. Results The mutation rate of p53 gene was 446% (33/74), of which 898% (27/73) showed point mutation, 182% (6/33) were fragment base deletion and 10 bp ~ 16bp. Allele heterozygosity deletion (LOH) mainly focused on exons 7 and 8, with 394% (13/33) and 273% (9/33), respectively. The incidence of mutations in exons 5 and 6 were 18.2% (6/33) and 15.1% (5/33), respectively. Exon 7RFLP analysis confirmed that mutation at position 249 (53.8%, 7/13) had a slight mutation at codon 248 (30.8%, 4/13). Immunohistochemistry showed that the overall detection rate of P53 protein overexpression was 703% (142/202). P53 protein was detected by pAb1801 and CM1 mAb.