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本研究旨在分析NPM1和FLT3-ITD突变与急性髓系白血病患者外周血白细胞数及骨髓原始细胞百分比的相关性。回顾分析我中心2009年1月至2011年12月份初治正常核型急性髓系白血病患者51例,其中男性22例,女性29例,中位年龄47岁(14-83岁)。采用聚合酶链式反应检测NPM1及FLT3-ITD突变状态。结果表明,与无NPM1突变患者相比,突变者初诊时外周血白细胞数较多(30.7×109/L vs 8.6×109/L,P=0.002);FLT3-ITD突变患者较无突变患者具有更多的外周血白细胞数(42.38×109/L vs 11.45×109/L,P=0.033)及更高的骨髓原始细胞百分比(74.0%vs 60.25%,P=0.036)。外周血白细胞数及骨髓原始细胞百分比在NPM1、FLT3-ITD无突变组、单独NPM1突变组、单独FLT3-ITD突变组到NPM1、FLT3-ITD双突变组逐步升高(均P<0.05)。白细胞数大于12.55×109/L的患者NPM1突变率明显升高(P=0.002),大于37.85×109/L者FLT3-ITD突变率明显升高(P=0.033);原始细胞比例大于72.25%的FLT3-ITD突变率明显升高(P=0.008)。NPM1突变患者首疗程完全缓解率(CR)明显高于无突变者(78.13%vs 40.0%,χ2=4.651,P=0.031)。结论:NPM1及FLT3-ITD突变患者白细胞计数及原始细胞比例大,提示NPM1与FLT3-ITD突变均可能促进白血病细胞增殖,且二者可能具有协同效应。
The purpose of this study was to investigate the association of NPM1 and FLT3-ITD mutations with peripheral blood leukocytes and bone marrow blasts in patients with acute myeloid leukemia. A retrospective analysis of our center in January 2009 to December 2011 initially treated patients with normal type AML, 51 patients, including 22 males and 29 females, the median age of 47 years (14-83 years old). Polymerase chain reaction was used to detect the mutation status of NPM1 and FLT3-ITD. The results showed that compared with patients without NPM1 mutation, the number of peripheral blood leukocytes was significantly higher in the newly diagnosed group (30.7 × 109 / L vs 8.6 × 109 / L, P = 0.002); patients with FLT3-ITD mutation had more (42.38 × 109 / L vs 11.45 × 109 / L, P = 0.033) and higher percentage of myeloid blasts (74.0% vs 60.25%, P = 0.036). The number of leukocytes in peripheral blood and the percentage of bone marrow blasts in NPM1, FLT3-ITD group, NPM1 group alone, FLT3-ITD group alone, NPM1 group and FLT3-ITD group were all increased gradually (all P <0.05). The mutation rate of NPM1 was significantly higher in patients with leukocyte count> 12.55 × 109 / L (P = 0.002). The mutation rate of FLT3-ITD was significantly higher than 37.85 × 109 / L (P = 0.033) FLT3-ITD mutation rate was significantly higher (P = 0.008). The first course of complete remission (CR) of patients with NPM1 mutation was significantly higher than that without mutation (78.13% vs 40.0%, χ2 = 4.651, P = 0.031). Conclusion: The leukocyte count and the percentage of blasts in patients with NPM1 and FLT3-ITD mutations are large, suggesting that both NPM1 and FLT3-ITD mutations may promote the proliferation of leukemic cells, and the two may have synergistic effects.