自发性破裂肝癌组织 CD16突变结构基因检测

目的：检测肝癌自发性破裂中 CD16结构基因突变，从分子水平更深入地探讨肝癌自发性破裂的机制。方法收集肝癌自发性破裂及非破裂患者各22例资料。患者肝癌组织中 CD16结构基因 S1、EC1和 EC2 DNA 突变情况应用PCR 法及基因测序技术进行检测。结果 EC1内第1483位、1533位及1605位出现 G/ A、G/ A 及 A/ G 等错义突变， EC2内在第5223位及5277位出现 T/ C 及 T/ G 等错义突变。Y5223H 及 Y5277F 两个错义位点突变率（54.54% vs 0）在两组之间差异有统计学意义（P <0.05），非破裂组 EC1及 EC2总的突变发生频率显著低于破裂组（ P <0.05）。结论FcγRⅢA 结构基因突变表面与肝癌巨噬细胞受体 CD16合成下降有关，是肝癌自发性破裂的可能机制。

Detection of the mutated structural gene of CD16 in ruptured HCC

Objective To explore the mechanism of spontaneous rupture of hepatocellular carcinoma(HCC)at the molecular level by detecting the mutation of CD16 structure gene. Methods In this study,22 specimens including 11 ruptured HCC and 11 non-ruptured HCC respectively were selected. The mutations of three exons including S1, EC1 and EC2,on genomic DNA of FcγRⅢA,were investigated by PCR and gene sequencing technologies. Re-sults Some heterozygous mutations were found in every exon of EC1,EC2 between the two groups,and it was sig-nificant on the differences of Y5223H and Y5277F mutations between the two groups(54. 54% vs 0)(P < 0. 05). The whole frequencies in exon EC1 were higher in ruptured HCC(P < 0. 05). Conclusion FcγRⅢA structural gene mutations are related with liver macrophage surface receptor CD16 decreased synthesis,and thus become pos-sible mechanism of spontaneous rupture of hepatocellular carcinoma.