CAJ | 학술논문

目的探索弥漫大B细胞淋巴瘤(DLBCL)的细胞因子信号转导抑制因子-1(SOCS-1)基因甲基化现象在DLBCL的发生、发展及预后中的意义.方法采用甲基化特异性聚合酶链反应(PCR)技术研究SOCS-1基因CpG岛的甲基化状态,运用实时荧光定量PCR方法定量分析SOCS-1基因的表达水平;收集30例DLBCL患者的临床资料,根据国际预后指数(IPI)分为低危组和高危组.结果 30例DLBCL患者中有17例(56.7%)SOCS-1基因呈启动子区甲基化,而对照组则无SOCS-1基因的甲基化现象.SOCS-1基因甲基化组的SOCS-1基因表达量与非甲基化组相比,其基因相对表达量明显减少(P＜0.05).与临床资料相结合,乳酸脱氢酶(LDH)升高组和结外病灶数＞1个的组中SOCS-1基因甲基化阳性率高于LDH正常组和结外病灶数≤1个组(P＜0.05).高危组的SOCS-1基因甲基化阳性率高于低危组(P＜0.05).结论 DLBCL患者中存在SOCS-1基因启动子区甲基化现象.SOCS-1基因甲基化后其表达水平受到抑制,提示SOCS-1基因及其甲基化在DLBCL的发生、发展中具有一定作用,并对DLBCL的预后有一定意义.
목적 탐색미만대B세포림파류(DLBCL)적세포인자신호전도억제인자-1(SOCS-1)기인갑기화현상재DLBCL적발생、발전급예후중적의의.방법 채용갑기화특이성취합매련반응(PCR)기술연구SOCS-1기인CpG도적갑기화상태,운용실시형광정량PCR방법정량분석SOCS-1기인적표체수평;수집30례DLBCL환자적림상자료,근거국제예후지수(IPI)분위저위조화고위조.결과 30례DLBCL환자중유17례(56.7%)SOCS-1기인정계동자구갑기화,이대조조칙무SOCS-1기인적갑기화현상.SOCS-1기인갑기화조적SOCS-1기인표체량여비갑기화조상비,기기인상대표체량명현감소(P＜0.05).여림상자료상결합,유산탈경매(LDH)승고조화결외병조수＞1개적조중SOCS-1기인갑기화양성솔고우LDH정상조화결외병조수≤1개조(P＜0.05).고위조적SOCS-1기인갑기화양성솔고우저위조(P＜0.05).결론 DLBCL환자중존재SOCS-1기인계동자구갑기화현상.SOCS-1기인갑기화후기표체수평수도억제,제시SOCS-1기인급기갑기화재DLBCL적발생、발전중구유일정작용,병대DLBCL적예후유일정의의.
Objective To explore the significance of the suppressor of cytokine signaling-1 (SOCS-1)gene methylation in the genesis, development and prognosis of diffuse large B-cell lymphoma (DLBCL).Methods The methylation state of CpG island in SOCS-1 gene were detected by methylation-specific polymerase chain reaction (PCR) and the level of SOCS-1 gene was measured by the real-time PCR. The clinical data of 30 patients with DLBCL were collected, and according to the international prognosis index (IPI), they were divided into low risk group and high risk group. Results Aberrant methylation of SOCS-1 in 17 DLBCL patients (56.7 %) were positive, however, in control group aberrant methylation was negative(P ＜0.01).The methylation level of DLBCL patients with positive SOCS-1 methylation was higher than that of patients with negative (P ＜0.05). Combined with the clinical data, the positive rate of methylation in patients with high level of serum LDH or the numbers of extra-nodal lesions＞l were significantly higher than that in patients with normal LDH level or the numbers of extra-nodal lesions ≤ 1, respectively. Hence, the positive rate of methylation in the high risk group of DLBCL was higher than that in the low risk group (P ＜0.05). Conclusion There were aberrant methylations of the SOCS-1 gene in the patients with DLBCL. The methylations of SOCS-1 can silence the gene expression, which indicates that SOCS-1 and its methylations play some role on genesis and development of DLBCL and can evaluate the prognosis of the patients with DLBCL.