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INT J LAB HEMATOL:219例慢性髓系白血病合并染色体异常和/或酪氨酸激酶域突变的结果

2019-01-27 MedSci MedSci原创

为了证实额外的染色体异常(ACAs)和激酶域(KD)突变在慢性髓系白血病(CML)患者进展和结局中的作用及其相互关系,研究人员分析了他们医院219例CML患者的ACAs和KD突变情况。研究人员通过中期细胞遗传学分析检测ACAs,通过测序BCR ABL1 KD检测KD突变。 结果显示24例患者(11.0%)发生ACAs, BCR ABL1或t(9;22)(q34;q11)易位。最常见的异常是8

为了证实额外的染色体异常(ACAs)和激酶域(KD)突变在慢性髓系白血病(CML)患者进展和结局中的作用及其相互关系,研究人员分析了他们医院219CML患者的ACAsKD突变情况。研究人员通过中期细胞遗传学分析检测ACAs,通过测序BCR ABL1 KD检测KD突变。

结果显示24例患者(11.0%)发生ACAs, BCR ABL1t(9;22)(q34;q11)易位。最常见的异常是8号染色体三体。53例伊马替尼耐药患者中13(24.5%)观察到12种不同的KD突变。p.(Y235H) (n = 3;23.07%) p.(F359V)p.(T315I) (n = 2;15.38%)出现频率最高。KD突变亚型(p.(E255K) p.(T315I) p.(F359V) p.(M244V)p.(L298V))ACAs共存。CML进展的发病率是12/22(54.5%)的患者留住和/KD突变和2/143(1.4%)的患者没有留住或KD突变(CI 95%,P < 0.001)KD突变组高于留住组(P = 0.046)ACAs/KD突变组的男性多于无ACAs/KD突变组(P = 0.013)

研究结果表明ACAs/KD突变与CML进展相关,是不良预后因素。它们的存在表现出性别差异,在男性中更为常见。当ACAsKD突变同时存在时,p.(E255K)p.(T315I)p.(F359V)p.(M244V)p.(L298V)出现的频率更高。

原始出处:

Mingming Xue Juan Cheng Jiangyun Zhao, Outcomes of 219 chronic myeloid leukaemia patients with additional chromosomal abnormalities and/or tyrosine kinase domain mutations

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    2019-01-29 fengyi812
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    2019-01-29 redcrab
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    2019-01-28 wxl882001

    了解一下

    0

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慢性髓性白血病(CML)是骨髓造血干细胞克隆性增殖形成的恶性肿瘤,占成人白血病的15%,全球年发病率为1.6~2/10万。1986至1988年在我国22个省(市、自治区)46个调查点进行的全国白血病发病情况调查显示CML的年发病率为0.36/10万。此后国内几个地区的流行病学调查显示CML的年发病率为0.39~0.55/10万。中国CML患者较西方国家更为年轻化,国内几个地区的流行病学调查显示

Blood:确诊时携带大量癌基因突变的慢性髓系白血病患者往往预后不良

目前我们对与慢性髓系白血病(CML)预后差相关的基因组事件尚知之甚少。Susan Branford等人对65位患者进行全外显子测序、拷贝数变异和/或RNA-测序,以检测在确诊时和急性期(BC)所存在的突变。46位有极端预后的慢性期患者在确诊后参与试验。在15位随后转入急性期或预后差的患者(总27位,56%)和3位治疗反应良好的患者(总19位,16%)中检测到癌基因变异(p=0.007)。确诊时频发

Lancet Oncol:慢性髓系白血病患者停止酪氨酸激酶抑制剂治疗的先决条件及对疾病控制的影响

研究认为对于实现深入治疗响应的慢性髓系白血病患者其主要致病分子标志物无响应率较高,可以停止酪氨酸激酶抑制剂治疗,特别是那些处于长期深入治疗响应的人群,可有效减少治疗的不良反应,降低医疗费用

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