Kelman Z, Prokocimer M, Peller S, Kahn Y, Rechavi G, Manor Y, Cohen A, Rotter V
Department of Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Blood. 1989 Nov 15;74(7):2318-24.
Molecular structural analysis of the p53 gene in patients with Philadelphia chromosome-positive chronic myelogenous leukemia (CML) indicates a significant incidence of gene rearrangements in patients at either accelerated phase or blastic crisis. Southern blot analysis of genomic DNA hybridizing with either genomic or cDNA p53 specific probes indicated that 30% of the CML patients at blastic crisis phase exhibited rearrangements, mostly mapping downstream to the first non-coding exon. This is compatible with the observation that the progression of CML from the chronic to the acute phase involves frequent aberrations in chromosome 17, to which the p53 oncogene has been mapped. Therefore, we suggest that one of the pathways of development of CML to the acute phase is associated with aberrations in the p53 nuclear oncogene.
对费城染色体阳性慢性粒细胞白血病（CML）患者的p53基因进行分子结构分析表明，处于加速期或急变期的患者中基因重排发生率显著。用基因组或cDNA p53特异性探针杂交基因组DNA的Southern印迹分析表明，30%的急变期CML患者存在重排，大多定位于第一个非编码外显子下游。这与以下观察结果相符，即CML从慢性期发展到急性期涉及17号染色体频繁畸变，p53癌基因已定位于该染色体。因此，我们认为CML发展到急性期的途径之一与p53核癌基因的畸变有关。
