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重组干扰素和阿糖胞苷治疗后慢性髓性白血病中一个极为罕见的克隆46,XY,del(7)(p12),t(9;22)(q34;q11)消失。

Disappearance of a highly unusual clone, 46,XY,del(7)(p12),t(9;22)(q34;q11) in chronic myeloid leukemia after treatment with recombinant interferon and cytosine arabinoside.

作者信息

Christodoulidou F, Silver R T, Macera M J, Verma R S

机构信息

Division of Hematology/Oncology, Long Island College Hospital--SUNY Health Science Center, Brooklyn 11201.

出版信息

Cancer Genet Cytogenet. 1992 Dec;64(2):174-7. doi: 10.1016/0165-4608(92)90351-8.

DOI:10.1016/0165-4608(92)90351-8
PMID:1486569
Abstract

A patient with the typical features of the stable phase of chronic myeloid leukemia (CML) displayed two karyotypically related subclones. In addition to the t(9;22), cells from one clone contained a deletion of the short arm of chromosome 7, del(7)(p12), [46,XY,del(7)(p12),t(9;22)(q34;q11)]; the other contained only the standard translocation [46,XY,t(9;22)(q34;q11)]. Cells with a deletion of the short arm of chromosome 7 at band p12 as the only additional abnormality have not been observed previously in CML. Conventional chemotherapy with hydroxyurea and then with recombinant interferon-alpha (rIFN-alpha) did not reduce the population of either subclone. However, after treatment with a combination of rIFN-alpha and low-dose cytosine arabinoside (LoDac) continuously infused subcutaneously (s.c.), cells from the clone with the deleted chromosome 7 disappeared and normal metaphases were demonstrable.

摘要

一名具有慢性髓性白血病(CML)稳定期典型特征的患者表现出两个核型相关的亚克隆。除了t(9;22)外,一个克隆的细胞含有7号染色体短臂缺失,即del(7)(p12),[46,XY,del(7)(p12),t(9;22)(q34;q11)];另一个克隆仅含有标准易位[46,XY,t(9;22)(q34;q11)]。7号染色体短臂p12带缺失作为唯一额外异常的细胞此前在CML中尚未观察到。先用羟基脲然后用重组α干扰素(rIFN-α)进行的传统化疗并未减少任一亚克隆的细胞群体。然而,在皮下持续输注rIFN-α和低剂量阿糖胞苷(LoDac)联合治疗后,具有7号染色体缺失的克隆的细胞消失,可检测到正常中期相。

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