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作 者:王娜[1] 潘健[1] 曹岚[1] 卢俊[1] 肖佩芳[1] 赵文理[1] 胡绍燕[1] 柴忆欢[1]
机构地区:[1]苏州大学附属儿童医院血液肿瘤科,215003
出 处:《中华血液学杂志》2013年第9期777-781,共5页Chinese Journal of Hematology
基 金:基金项目:国家“十一五”科技支撑计划项目(2007BAI04803);国家自然科学基金(81100371)
摘 要:目的检测miR-203在儿童急性白血病患者中的甲基化状态及表达情况,探讨其临床意义。方法应用甲基化特异性聚合酶链反应检测miR-203启动子区CpG岛的甲基化状态,用实时荧光定量聚合酶链反应检测miR-203的相对表达量,分析其与临床指标间的关系。结果31例儿童急性淋巴细胞白血病(ALL)、15例儿童急性髓系白血病(AML)及23份非恶性血液病患儿骨髓标本(对照组)均未检测到miR-203的甲基化现象。miR-203在对照组、儿童急性白血病组、ALL组及AML组的相对表达量分别为16.93±6.31、48.97±10.38、55.88±12.91、24.28±9.10,儿童急性白血病组、ALL组与对照组相比,差异有统计学意义(P值分别为0.01和0.009),儿童AML组与对照组相比,差异无统计学意义(P=-0.514)。各项临床指标中,miR-203的表达与初诊ALL患儿的性别、免疫分型、染色体核型、是否检出融合基因、BCR—ABL基因表达、SIL-TAL1基因表达、泼尼松试验及急性白血病患儿的性别、染色体核型、是否检出融合基因、SIL—TAL1基因表达相关(P值均〈0.05)。其中在ALL危险度分组两两比较中,中危组与高危组两组间miR-203的表达差异有统计学意义(P=0.022)。结论miR-203在大部分急性白血病患儿中不受甲基化机制调控。miR.203可能作为原癌基因参与儿童急性白血病尤其是ALL的形成。miR-203的高表达可能与急性白血病患儿尤其是ALL患儿的不良预后相关。Objective To investigate the methylation, expression and clinical significance ofmiR- 203 in pediatric acute leukemia. Methods The methylation status of miR-203 promoter CpG islands was detected with methylation-specific polymerase chain reaction. The expression of miR-203 was detected by Taqman real-time quantitative polymerase chain reaction. And the clinical significance of miR-203 in pediatric acute leukemia (ALL) was also analyzed. Results The promoter of miR-203 was unmethylated in all of 31 pediatric acute lymphoblastic leukemia, all of 15 pediatric acute myeloid leukemia(AML) and all of 23 controls. The relative expression levels of miR-203 in controls, pediatric acute leukemia, ALL and AML were 16.93-4-6.31, 48.974-10.38, 55.88+12.91, 24.28+9.10 respectively. The results indicated that miR- 203 was significantly up-regulated in pediatric acute leukemia (P=0.011) and ALL (P=0.009), not in pediatric AML (P=-0.514) compared with control. The expression ofmiR-203 was significantly related with the gender, immunophenotype, chromosome, fusion gene, BCR-ABL, SIL-TALl and prednisone experiment in pediatric ALL and the gender, chromosome, fusion gene, SIL-TALl in pediatric acute leukemia (P〈0.05). And in risk stratification pairwise comparisons, the expression of miR-203 in the medium-risk and high-risk groups appeared significantly different (P=-0.022). Conclusions miR-203 may not be regulated with methylation mechanism in pediatric acute leukemia, miR-203 may be a proto- oncogene involved in the formation of pediatric acute leukemia and ALL. Further analyses indicated that high expression of miR-203 may be associated with poor prognosis of pediatric ALL and acute leukemia.
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