首页> 外文期刊>Leukemia Research: A Forum for Studies on Leukemia and Normal Hemopoiesis >Erythroblastic and/or megakaryocytic dysplasia in de novo acute myeloid leukemias M0-M5 show relation to myelodysplastic syndromes and delimit two main categories.
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Erythroblastic and/or megakaryocytic dysplasia in de novo acute myeloid leukemias M0-M5 show relation to myelodysplastic syndromes and delimit two main categories.

机译:从头开始的急性髓细胞性白血病M0-M5中的红细胞增生和/或巨核细胞增生异常与骨髓增生异常综合征相关,并界定了两个主要类别。

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Erythroblastic and/or megakaryocytic dysplasia (EMD) was evaluated in diagnostic bone marrow smears of 43 consecutively treated patients under 65 years with de novo acute myeloid leukemia (AML) M0-M5 according to FAB criteria. The evaluation was possible in 39 (91%) patients, i.e. in 32 of 34 patients with non-M3 AML treated in the study UHKT-911 and seven of nine cases with AML M3 treated in other studies. Among non-M3 AML 15 patients were categorized without EMD and 17 cases with EMD. Cytogenetic abnormalities of chromosome 5, 7, 3 or a complex karyotype were found in eight of 17 patients with EMD and in one of 15 cases without EMD (P = 0.018). Seven patients in each category exhibited a normal karyotype. Classical induction therapy with three to four doses of daunorubicin 45 mg/m2 and standard doses of cytosine arabinoside (AraC) for 7 days lead to complete remission in 11 of 14 (78.6%) cases without EMD but only in four of 14 (28.6%) cases with EMD (P = 0.021). High doses (2000 mg/m2 per 12-h x 10) of AraC plus daunorubicin induced complete remission in seven of 10 patients with EMD. Patients with EMD showed significantly worse overall survival (P = 0.03) with a median 13.5 months, while the median survival was estimated to 68.7 months in cases without EMD. The dysplastic features of EMD, karyotypes typical for myelodysplastic syndromes (MDS), poor response to classical therapy and survival show a relation of AML with EMD to MDS. AML without EMD may represent a different biological favorable category.
机译:根据FAB标准,对65岁以下连续接受治疗的43岁新发急性髓细胞性白血病(AML)M0-M5的连续治疗患者的诊断性骨髓涂片评估了促红细胞生成和/或巨核细胞增生异常(EMD)。在39例(91%)患者中进行了评估,即在研究UHKT-911中治疗的34例非M3 AML患者中有32例在其他研究中治疗的9例AML M3患者中有7例可以进行评估。在非M3 AML患者中,有15例没有EMD,17例有EMD。在17例有EMD的患者中有8例和15例无EMD的患者中发现了5、7、3号染色体或复杂核型的细胞遗传学异常(P = 0.018)。每个类别中有7名患者表现出正常的核型。经典诱导疗法采用三到四剂柔红霉素45 mg / m2和标准剂量的胞嘧啶阿拉伯糖苷(AraC)治疗7天,在没有EMD的14例中有11例(78.6%)完全缓解,但在14例中有4例(28.6%)完全缓解。 )患有EMD的病例(P = 0.021)。高剂量(2000 mg / m2每12-h x 10)AraC加柔红霉素可导致10名EMD患者中的7名完全缓解。患有EMD的患者的总生存期显着变差(P = 0.03),中位数为13.5个月,而没有EMD的患者的中位生存期估计为68.7个月。 EMD的异常增生,典型的骨髓增生异常综合征(MDS)的核型,对经典疗法的不良反应和生存率均显示AML和EMD与MDS的关系。没有EMD的AML可能代表了不同的生物学优势类别。

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