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大多数(>90%)慢粒(CML)患者有标准的9和22号染色体的易位,导致费城染色体的形成。具复杂易位染色体的起因,也是由于bcr/abl基因融合的结果,这种基因融合,细胞遗传学水平尚无法观察。众所公认,存在于9 q34的癌基因abl易位到22q11的断裂丛集区(bcr),形成异常的基因,在一些患者是所谓Ph阴性慢粒。特别有兴趣的是Ph阴性和有额外染色体参与的不寻常或变异的易位,本文提供一例以前未见报道的Ph阴性慢粒的变异易位,细胞遗
Most (>90%) patients with chronic granuloma (CML) have standard 9 and 22 chromosome translocations that result in the formation of Philadelphia chromosomes. The cause of chromosomes with complex translocations is also the result of the bcr/abl gene fusion. This kind of gene fusion cannot be observed at the cytogenetic level. It is generally accepted that the oncogene abl exists in the 9q34 translocation to the 22q11 cleavage cluster region (bcr), forming an abnormal gene, and in some patients it is a so-called Ph-negative slow particle. Of particular interest is the unusual or variable translocation of Ph-negative and extra chromosome involvement. This article provides an example of a previously reported mutational translocation of Ph-negative slow-grain cells.