Donti E, Tabilio A, Donti G V, Carotti A, Falsetti F, Rosetti A
Leuk Res. 1985;9(9):1149-53. doi: 10.1016/0145-2126(85)90105-5.
Cytogenetic analysis of bone marrow from a chronic myeloid leukemia patient in chronic phase revealed a classical Philadelphia chromosome from a complex translocation t(2;9;22). The break points on 9 and 22 were, apparently, the same as for the standard translocation (9;22). However, whereas the terminal band of 9 (9q34) was translocated in the usual site, that is on 22q-, the tract deleted from 22 was present on band p13 of chromosome 2. The finding of this rare 22 translocation in classical CML would seem to support the hypothesis that the crucial event in the pathogenesis of CML is the translocation of band 9q34, that contains the c-abl oncogene, onto the Ph' chromosome, rather than the translocation of the tract deleted from 22 to some other chromosome site.
对一名慢性期慢性髓性白血病患者的骨髓进行细胞遗传学分析发现，其复杂易位t(2;9;22)产生了典型的费城染色体。9号和22号染色体上的断点显然与标准易位(9;22)相同。然而，虽然9号染色体的末端带(9q34)易位到了通常的位置，即在22号染色体长臂，但从22号染色体缺失的片段却出现在2号染色体的p13带上。在经典慢性髓性白血病中发现这种罕见的22号染色体易位似乎支持了这样一种假说，即慢性髓性白血病发病机制中的关键事件是包含c-abl癌基因的9q34带易位到费城染色体上，而不是从22号染色体缺失的片段易位到其他染色体位点。
