摘要
目的 :探讨 AL L 和各亚型中 P16基因失活和纯合缺失的发生率及 m RNA表达。方法 :对 40例AL L (B- AL L2 8例 ,T- AL L7例 ,前 B- AL L5例 )和 15例对照组骨髓标本 ,采用 PCR法检测 P16基因的纯合缺失 ,REP法检测 P16基因的高度甲基化 ,RT- Nest- PCR法检测其 m RNA的表达。结果 :AL L P16基因高度甲基化或纯合缺失发生率为 80 % ,而对照组无一例 P16基因失活 ;T- AL L中 P16基因纯合缺失高于高度甲基化 ;B- AL L中高度甲基化多于纯合缺失。 5例 P16基因高度甲基化尚有 m RNA表达 ,其余均无表达。结论 :P16基因的异常是 AL L 的主要发病机制之一。 T- AL L P16基因的纯合缺失为主要表现 ,而 B- AL L P16的高度甲基化为主要表现。同时 ,无论 P16基因纯合缺失或高度甲基化 ,均能高度抑制 m
Objective:To explore incidence of P16 gene inactivation and homozygous deletion and the expression of mRNA in ALL and various subtypes. Methods:The homozygous delete of P16 gene was determinated by PCR,hypermethylation by REP and the expression of P16 gene by RT Nest PCR .Results:In ALL, the incidence of P16 hypermethylation or homozygous deletion is 80%,there is no abnormal in control. In T ALL, homozygous delete of P16 gene is more common than hypermethylation. In B ALL, hypermethylation of P16 gene is higher than homozygous deletion.Hypermethylation mRNA expression exists in 5 cases with P16 gene,but not in the others. Conclusion:Abnormal P16 gene is the main pathogenesis in ALL. In T ALL, P16 gene homozygous delete is predominant epitope, and in B ALL, however, hypermethylation of P16 gene is predominant presentation. Meanwhile both homozygous deletion and hypermethylation of P16 gene can strongly inhibit mRNA expression. [FK(WB80011。5]
出处
《温州医学院学报》
CAS
2000年第1期5-7,共3页
Journal of Wenzhou Medical College
基金
浙江省卫生厅科研基金!课题 ( 98B0 65
关键词
急性白血病
淋巴细胞性
P16基因
mRNA
leukemia
acute lymphatic leukemia
P16 gene
homozygous deletion hypermethylation
expression of mRNA