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出 处:《中华医学遗传学杂志》2016年第2期155-159,共5页Chinese Journal of Medical Genetics
基 金:浙江省医药卫生科技计划项目(2014KYB233);宁波市医学科技计划项目(2009801);宁波市自然科学基金(2012A610194)
摘 要:目的探讨急性髓系白血病(acutemyeloidleukemia,AML)患者中抑癌基因p15反义RNA(p15AS)的表达及其临床意义。方法应用单链特异引物逆转录的实时定量PCR方法验证AML细胞系存在p15AS,分析43例AML患者和21例良性血液病患者(对照组)骨髓p15AS和p15mRNA的表达水平,并分析p15AS的表达量与AML临床特征的关系。应用流式细胞术检测AML患者和对照组骨髓中p15蛋白的表达。结果急性髓系白血病细胞系中存在p15AS高表达。与对照组相比,AML患者p15AS表达增加而p15mRNA表达下调(t=41.45,P=0.000;t=-24.76,P=0.000)。AML组骨髓细胞中p15蛋白的表达[13.2%(10.2%~18.50%)]较对照组E84.5%(80.25%~86.8%)]显著减少,差异有统计学意义(Z=-6.22,P=0.000)。P15AS表达水平与AML患者的性别、年龄、FAB分型、初诊白细胞计数、血小板数量、骨髓增生程度和细胞遗传学预后分组无相关性(均P〉0.05)。结论p15AS高表达可能是AML的常见事件,并可能在抑癌基因p15表观遗传沉默中具有重要作用。Objective To detect the presence of p15 antisense RNA (pl5AS) in acute myeloid leukemia (AML). Methods pl5AS and p15 mRNA in two leukemia cell lines was detected with strand- specific primer RT-qPCR. To explore the connection between p15AS and AML, 43 patients with newly diagnosed AML and 21 patients with benign diseases (Iron deficiency anemia) as controls were enrolled. The expression level of p15AS in bone marrow cells derived from the patients and the controls were determined by strand-specific primer RT-qPCR, and its relationship with clinical features was analyzed. Results The two AML lines displayed high pl5AS and low p15 expression. Samples derived from the AML patients showed relatively increased expression of p15AS and down-regulated p15 expression in their bone cells. In contrast, the 21 controls showed high expression of p15 but relatively low expression of the p15AS. Compared with the normal controls, the expression levels of p15 protein were significantly lower among the AML patients (P〈0.01). No relationships were detected between the level of pl5AS and the patient's age, gender, FAB subtype, total white blood cell count, platelet count, proliferative degree of bone marrow cell and karyotype classification (P〉0.05 for all comparisons). Conclusion High expression of p15 antisense RNA was frequently found among AML patients, and may play an important role in epigenetic silencing of p15.
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