Popenoe D W, Schaefer-Rego K, Mears J G, Bank A, Leibowitz D
Blood. 1986 Nov;68(5):1123-8.
Chromosomal translocation is one mechanism by which cellular oncogenes may be activated during tumorigenesis. The translocation of the abl oncogene to the Philadelphia chromosome in chronic myelogenous leukemia (CML) results in a new RNA transcript that fuses sequence from chromosome 22 to sequence from the abl oncogene. This RNA presumably codes for a new abl-related protein product found in CML, the activity of which is different from the normal abl protein. The molecular structure of the translocation varies from patient to patient, and the individual variation in RNA transcript and protein product remains to be defined. This report describes the frequent occurrence of chromosomal deletion within the 9q+ chromosome during these translocations. The location of the deletions suggests that some mechanism maintains the chromosomal breakpoint on the Philadelphia chromosome within a limited region. These deletions complicate the interpretation of Southern blots as a means of detecting the translocation.
染色体易位是一种在肿瘤发生过程中细胞癌基因可能被激活的机制。在慢性粒细胞白血病（CML）中，abl癌基因易位至费城染色体，导致一种新的RNA转录本产生，该转录本将22号染色体的序列与abl癌基因的序列融合。这种RNA可能编码一种在CML中发现的新的abl相关蛋白产物，其活性与正常abl蛋白不同。易位的分子结构因患者而异，RNA转录本和蛋白产物的个体差异仍有待确定。本报告描述了在这些易位过程中9q +染色体上频繁发生的染色体缺失。缺失的位置表明，某种机制将费城染色体上的染色体断点维持在一个有限的区域内。这些缺失使作为检测易位手段的Southern印迹的解释变得复杂。
