P53 IN CHRONIC MYELOGENOUS LEUKEMIA IN ACUTE PHASE
P53 IN CHRONIC MYELOGENOUS LEUKEMIA IN ACUTE PHASE
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DOI：
10.1073/pnas.88.14.6293
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发表时间：
1991-07-01
影响因子：
11.1
通讯作者：
CANAANI, E
中科院分区：
文献类型：
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作者：
FEINSTEIN, E;CIMINO, G;CANAANI, E
所有慢性粒细胞白血病(CML)患者都经历了从慢性到急性期的临床过渡。这种转变通常与以I(17q)异常形式存在的17号染色体短臂的缺失有关。由于P53基因是一种抑制基因，位于17p13，我们研究了它在CML进展过程中失活的可能性。因此，我们对大量CML急性期患者白血病细胞中P53的结构和表达进行了研究。我们发现，尽管该基因很少重排，但在具有I(17q)异常的患者以及一些没有核型变化的患者中，一个p53等位基因完全缺失。在所有这些患者中，剩余的等位基因因表达丧失、重排或点突变而失活。对一些同时携带P53等位基因的患者的详细分析表明，既没有表达丢失，也没有结构变化。研究表明，P53功能的丧失与大约25%的CML患者的进展有关。
All patients with chronic myelogenous leukemia (CML) undergo clinical transition from chronic to acute phase. This transition is often associated with deletion of the short arm of chromosome 17 in the form of the i(17q) aberration. Since the p53 gene is a suppressor gene and is located on 17p13, we examined the possibility that it is inactivated during progression of CML. Therefore, we studied the structure and expression of p53 in the leukemic cells of a large number of CML patients in acute phase. We found that although the gene is rarely rearranged, one p53 allele is completely deleted in patients with the i(17q) aberration as well as in some patients who do not show karyotypic changes. In all of these patients the remaining allele is inactivated through loss of expression, rearrangement, or point mutation. Detailed analysis of some patients who carry both p53 alleles indicated neither loss of expression nor structural alterations. It appears that p53 loss of function is associated with progression of around 25% of CML patients.