摘要
目的:探讨p16基因家族失活与白血病发生、发展及预后的关系。方法:PCR检测p16、p15、p18、p19 基因在白血病中纯合子缺失。结果:p16、p15 基因外显子1在AL组纯合子缺失率分别为22.37 %、17.05 %,在ALL组为45.95 %、32.43 %,在ANLL组均为5.88 %;在CML的慢性期均为0。p16、p15基因外显子2在AL组纯合子缺失率分别为12.5 %、5.68 %;在ALL组为24.32 % 、10.81 %;在ANLL组为3.92 %、1.96 %;在CML和对照组二者均无缺失。p18、p19 基因外显子1在AL组纯合子缺失率分别为1.14 %、0;在ALL组分别为2.70 %、0;在ANLL和对照组均无缺失。结论:p16、p15基因纯合子缺失在AL的发生频率较高,ALL缺失率明显高于ANLL,复发ALL组基因失活率最高。p16、p15基因纯合子缺失是AL,尤其是ALL的发病重要因素之一。p18、p19基因在AL组中几乎未见纯合子缺失。在ALL中,p16纯合子缺失率高于p15纯合子缺失率。两个基因的纯合子缺失常伴随存在。在ANLL中,p16、p15基因的纯合子缺失均少见。
Objective: To explore the correlation between the family of p16 gene inactivation and generation, prognosis of leukemia, and then to clarify, the pathogenesis of leukemia, to inspect process of leukemia. Methods: Used polymerase chain reaction(PCR) to study p16, p15,p18,p19 gene homozygous deletion in leukemia. Results: Homozyous deletion of p16,p15 gene exon 1 was found 22.37 %,17.05 % in AL, respectively. Homozyous deletion of p16, p15 gene exon 1 was found 45.95 %, 32.43 % in ALL, respectively. It was all found 5.88 % in ANLL. But that of p16 and p15 gene exon 1 was found 0 % in CML (chromic period). Homozygons deletion of p16 and p15 gene exon 2 was found 12.5 %, 5.68 in AL, respectively. In ALL, it was 24.32 % and 10.81 %. In ANLL, it was 3.92 % and 1.96 %. There was no homozygousdeletion in chronic period and in blast crisis of CML and the controls. Conclusion: Homozyous deletion of rates of p16 and p15 in ALL were higher than in ANLL. It were highest in replase cases,especially. p16 and p15 gene homozygous deletion plays an important role in generation and development in AL ,especially in ALL. There was nearly deletion of p18 and p19 gene found in AL. Homozygous deletion rate of p16 gene was higher than that in p15 gene. Homozygous deletion of p15 gene was company with p16 gene. Homozygous deletion of p16 and p15 gene was infrequent in ANLL.
出处
《白血病．淋巴瘤》
CAS
2004年第5期280-282,共3页
Journal of Leukemia & Lymphoma
