Fainstein E, Marcelle C, Rosner A, Canaani E, Gale R P, Dreazen O, Smith S D, Croce C M
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
Nature. 1987;330(6146):386-8. doi: 10.1038/330386a0.
The leukaemic cells of more than 90% of chronic myelogenous leukaemia (CML) patients and of 10% of acute lymphocytic leukaemia (ALL) patients carry the t(9:22) (q34:q11) translocation which generates the Philadelphia chromosome (Ph1). In CML the abl gene is translocated from chromosome 9 to the centre of the bcr gene on chromosome 22 and this results in production of chimaeric bcr-abl RNA translated into a protein of relative molecular mass (Mr) 210,000 (210K). Our data indicate that in ALL abl is translocated into the 5' region of the bcr gene. The consequence of this is the expression of a fused transcript in which the first exon of bcr is linked to the second abl exon. This transcript encodes a 190K protein kinase.
超过90%的慢性粒细胞白血病(CML)患者以及10%的急性淋巴细胞白血病(ALL)患者的白血病细胞携带t(9:22) (q34:q11)易位,该易位产生费城染色体(Ph1)。在CML中,abl基因从9号染色体易位至22号染色体上bcr基因的中心位置,这导致嵌合性bcr-abl RNA的产生,该RNA被翻译为相对分子质量(Mr)为210,000(210K)的蛋白质。我们的数据表明,在ALL中,abl易位至bcr基因的5'区域。其结果是表达一种融合转录本,其中bcr的第一个外显子与abl的第二个外显子相连。该转录本编码一种190K的蛋白激酶。