论文部分内容阅读
目的检测弥漫性大B细胞性淋巴瘤(DLBCL)中A20基因甲基化状况,探讨其对DLBCL临床过程及预后的影响。方法通过组织学观察及免疫表型检测筛选104例DLBCL,收集其临床病理资料及随访;并以甲基化特异性PCR(MSP)法检测A20基因启动子区5’Cp G岛甲基化的情况;以免疫组化SP法检测肿瘤细胞P糖蛋白(Pg P)和Ki-67蛋白的表达。结果 104例DLBCL中,A20基因甲基化率为26%(27/104),活化后B细胞样(ABC)-DLBCL组甲基化率(35.4%)高于生发中心B细胞样(GCB)DLBCL组(10.2%)(P<0.05);Pg P阳性率65.4%(68/104),A20基因甲基化组Pg P阳性率(85.2%)明显高于无甲基化组(58.4%)(P<0.05);A20基因甲基化与非甲基化组之间Ki-67高表达病例与低表达病例均无明显差异(P>0.05);A20基因甲基化病例的复发率明显高于无甲基化病例(P<0.05);生存分析发现,两组病例的生存状况差异不显著。结论 DLBCL部分病例存在A20基因甲基化,以ABC-DBLCL病例多见。A20基因甲基化与DLBCL的复发有关,且可能通过NF-κB异常活化而促进肿瘤细胞Pg P蛋白表达,从而影响DLBCL的化疗效果。
Objective To investigate the methylation status of A20 gene in diffuse large B cell lymphoma (DLBCL) and to explore its influence on the clinical course and prognosis of DLBCL. Methods 104 cases of DLBCL were screened by histological observation and immunophenotyping. The clinical and pathological data were collected and followed up. Methylation-specific methylation of 5’Cp G island was detected by methylation-specific PCR (MSP) The expression of Pgp and Ki-67 in tumor cells was detected by immunohistochemical SP method. Results The methylation rate of A20 gene was 26% (27/104) in 104 cases of DLBCL. The methylation rate of 35.6% in B cell line (ABC) -DLBCL group was higher than that in germinal center B cell sample (GCB) The positive rate of Pg P was 65.4% (68/104) in DLBCL group (P <0.05), and the positive rate of Pg P in methylation group was significantly higher than that in DLBCL group (85.2% vs 58.4% (P <0.05). There was no significant difference in the expression of Ki-67 between methylated and unmethylated A20 (P> 0.05), and the methylation of A20 was significantly higher There was no methylation (P <0.05). Survival analysis showed that there was no significant difference in survival between the two groups. Conclusion A20 gene methylation exists in some cases of DLBCL, which is more common in ABC-DBLCL cases. Methylation of A20 gene is associated with the recurrence of DLBCL, and may promote the expression of Pg P protein in tumor cells through the abnormal activation of NF-κB, thus affecting the chemotherapeutic effect of DLBCL.