CAJ | 학술논문

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。
목적：검측간암자발성파렬중 CD16결구기인돌변，종분자수평경심입지탐토간암자발성파렬적궤제。방법수집간암자발성파렬급비파렬환자각22례자료。환자간암조직중 CD16결구기인 S1、EC1화 EC2 DNA 돌변정황응용PCR 법급기인측서기술진행검측。결과 EC1내제1483위、1533위급1605위출현 G/ A、G/ A 급 A/ G 등착의돌변， EC2내재제5223위급5277위출현 T/ C 급 T/ G 등착의돌변。Y5223H 급 Y5277F 량개착의위점돌변솔（54.54% vs 0）재량조지간차이유통계학의의（P <0.05），비파렬조 EC1급 EC2총적돌변발생빈솔현저저우파렬조（ P <0.05）。결론FcγRⅢA 결구기인돌변표면여간암거서세포수체 CD16합성하강유관，시간암자발성파렬적가능궤제。
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.