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作 者:唐玉珠[1] 杨渝珍[2] 陈春莲[3] 尤颖健[4] 龚维龙[1] 邹萍[1]
机构地区:[1]同济医科大学附属协和医院血液病研究所,武汉430022 [2]同济医科大学实验医学中心分子生物学研究室,武汉430030 [3]同济医科大学附属同济医院病理室,武汉430030 [4]同济医科大学基础医学院生物化学教研室,武汉430030
出 处:《同济医科大学学报》1998年第1期31-34,共4页Acta Universitatis Medicinae Tongji
基 金:国家自然科学基金资助项目(No.3918008)
摘 要:应用PCR- SSCP、Northern blot和免疫细胞化学方法,对30例临床各期慢性粒细胞性白血病(CML)和K562、HL-60细胞系进行p53基因突变与表达的研究。结果发现,17例慢性期CML中仪1例有外显子6的突变和细胞内P53蛋白的聚积,所有病例均可检测到p53的mRNA表达。而4例加速期和9例急变期CML中各有2例分别在外显子5、6、7上发现突变,有p53表达的仅7例,1例加速期患者的P53蛋白呈强阳性。K562和HL-60细胞系中P53蛋白和mRNA均呈阴性。CML恶化进程中p53基因突变和表达频率的改变表明P53基因的改变至少在部分CML急变中起着重要作用。30 cases of chronic myelogenous leukemia ( CML ) at various phases and two cell lines of K562. HL-60 were studied by means of PCR-SSCP, Northern blot hybridization and immunocytochemical stain. In one of the 17 cases in chronic phase (CP), we found a p53 mutation in exon 6 and a high level of P53 protein in the white blood cells. All of the 17 cases had detectable levels of p53 mRNA in Northern blot hybridization. But studies on the more acute phase of CML showed a different result from the chronic phase. The abnormal migration bands of PCR-SSCP were found in 2 of 4 accelerated phase (AP) and 2 of 9 blast cri-sis (BC) patients, respectively, in the p53 exons 5, 6 and 7. 1mmunocytochemistry showed a positive stain of p53 in one of these accelerated cases. P53 transcript can not be detected almost in half of them (6/13). The K562 and HL-60 cell lines also showed negative findings on P53 mRNA and protein. We can conclude from the distinctive rates of p53 mutation and expression between chronic phase and more acute phase that the al-teration of p53 gene may play an important role in many evolutions of CML to blast crisis.
分 类 号:R733.720.2[医药卫生—肿瘤]
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