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在很多伴有人体肿瘤发生的染色体异常中,最常见的是Ph染色体,至少90%的慢性粒细胞白血病(CML)患者带有这条染色体,它来源于9号和22号染色体之间的易位(臂间交换).长期以来,人们就怀疑正是这个易位激活了一个细胞癌基因,这个癌基因再刺激骨髓干细胞及其后代使其毫无控制地增殖.三年多以前已由鼠Abelson-白血病病毒的癌基因(v-abl)〔它是细胞原癌基因(c-abl)的同源物〕确定.在CML病人中含有这个c-abl.但是易位怎样改变这个abl基因,人们并不清楚.现在Shtivelman等和Heister-Kamp等提出:易位使c-abl
In many chromosomal abnormalities with human tumors, the most common is the Ph chromosome. At least 90% of patients with CML have this chromosome. It is derived from the easy between chromosome 9 and chromosome 22. Position (arm-to-arm exchange). It has long been suspected that this translocation activates a cell oncogene that stimulates bone marrow stem cells and their progeny to proliferate without control. It has been more than three years ago. The Abelson-Leukemia virus oncogene (v-abl), which is a homologue of the cellular proto-oncogene (c-abl), is identified in patients with CML, but how the translocation alters this abl gene, People are not clear. Now Shtivelman et al. and Heister-Kamp et al. proposed: Translocation makes c-abl