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利用腺苷酸激酶-1多态性在体细胞杂种中证实慢性髓性白血病中费城染色体易位的克隆起源。

Clonal origin of the Philadelphia translocation in chronic myeloid leukemia demonstrated in somatic cell hybrids using an adenylate kinase-1 polymorphism.

作者信息

Geurts van Kessel A H, van Agthoven A J, Hagemeijer A

出版信息

Cancer Genet Cytogenet. 1982 May;6(1):55-8. doi: 10.1016/0165-4608(82)90021-8.

Abstract

Hybrid cell lines were derived from fusion of rodent cells with leukocytes from a t(9q+; 22q-)-positive chronic myeloid leukemia (CML) patient carrying a chromosome No. 9-linked adenylate kinase-1 (AK1) polymorphism (AK1 1-2). The AK12 allele was consistently expressed when 9q+ was present, whereas the AK11-coded isozyme was formed when the normal chromosome No. 9 was present. These results provide additional data confirming the clonal origin of the Ph1 translocation in CML.

摘要

杂交细胞系源自啮齿动物细胞与一名携带9号染色体连锁腺苷酸激酶-1(AK1)多态性(AK1 1-2)的t(9q+; 22q-)阳性慢性髓性白血病(CML)患者的白细胞的融合。当存在9q+时,AK12等位基因持续表达,而当存在正常9号染色体时,则形成AK11编码的同工酶。这些结果提供了额外的数据,证实了CML中Ph1易位的克隆起源。

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