Prenatal origin of childhood AML occurs less frequently than in childhood ALL.
Prenatal origin of childhood AML occurs less frequently than in childhood ALL.
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儿童 AML 的产前起源比儿童 ALL 的发生率要低。
DOI：
10.1186/1471-2407-6-100
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发表时间：
2006-04-21
期刊：
影响因子：
3.8
通讯作者：
Zuna J
中科院分区：
文献类型：
--
作者：
Burjanivova T;Madzo J;Muzikova K;Meyer C;Schneider B;Votava F;Marschalek R;Stary J;Trka J;Zuna J
虽然儿童急性淋巴细胞白血病（ALL）有足够令人信服的证据，但关于儿童急性髓细胞白血病（AML）的产前起源的数据并不全面。我们的研究旨在筛选非婴儿儿童AML和ALL患者的古特里卡（新生儿血斑），以确定其各自白血病标志物的存在。我们分析了12例2-6岁ALL患者的古特里卡，使用免疫球蛋白（IG）和T细胞受体（TCR）基因重排（n = 15）和/或TEL/AML 1融合基因的内含子断点（n = 3）。在AML患者（n = 13，年龄1-14岁）中，PML/RAR α（n = 4）、CBF β/MYH 11（n = 3）、AML 1/ETO（n = 2）、MLL/AF 6（n = 1）、MLL/AF 9（n = 1）和MLL/AF 10（n = 1）融合基因和/或FLT 3基因的内部串联重复（FLT 3/ITD）（n = 2）用作克隆型标志物。使用患者DNA到健康供体DNA中的系列稀释液确定的测定灵敏度允许我们检测古特里卡中的白血病前克隆，前提是新生儿血斑中存在1-3个阳性细胞。在3例ALL患者（25%）中，我们在古特里卡中重复检测了他们的白血病标志物（IG/TCR n = 2; TEL/AML 1 n = 1）。我们没有在任何AML患者中发现患者特异性分子标志物。在迄今为止检查的最大队列中，我们使用相同的方法对非婴儿儿童ALL和AML进行回溯。我们的数据表明，与ALL病例相比，AML的产前起源较不常见，或者出生时AML的前白血病细胞负荷显著较低。
While there is enough convincing evidence in childhood acute lymphoblastic leukemia (ALL), the data on the pre-natal origin in childhood acute myeloid leukemia (AML) are less comprehensive. Our study aimed to screen Guthrie cards (neonatal blood spots) of non-infant childhood AML and ALL patients for the presence of their respective leukemic markers. We analysed Guthrie cards of 12 ALL patients aged 2–6 years using immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangements (n = 15) and/or intronic breakpoints of TEL/AML1 fusion gene (n = 3). In AML patients (n = 13, age 1–14 years) PML/RARalpha (n = 4), CBFbeta/MYH11 (n = 3), AML1/ETO (n = 2), MLL/AF6 (n = 1), MLL/AF9 (n = 1) and MLL/AF10 (n = 1) fusion genes and/or internal tandem duplication of FLT3 gene (FLT3/ITD) (n = 2) were used as clonotypic markers. Assay sensitivity determined using serial dilutions of patient DNA into the DNA of a healthy donor allowed us to detect the pre-leukemic clone in Guthrie card providing 1–3 positive cells were present in the neonatal blood spot. In 3 patients with ALL (25%) we reproducibly detected their leukemic markers (Ig/TCR n = 2; TEL/AML1 n = 1) in the Guthrie card. We did not find patient-specific molecular markers in any patient with AML. In the largest cohort examined so far we used identical approach for the backtracking of non-infant childhood ALL and AML. Our data suggest that either the prenatal origin of AML is less frequent or the load of pre-leukemic cells is significantly lower at birth in AML compared to ALL cases.
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