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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 RNA的表达
Objective: To investigate the incidence of inactivation and homozygous deletion of p16 gene and expression of m RNA in AL L and subtypes. METHODS: Homozygous deletion of P16 gene was detected by PCR in 40 cases of AL L (B-AL L2 8 cases, T-AL L7 cases, pre-B-AL L5 cases) and 15 cases of control group. REP assay The hypermethylation of P16 gene was detected by RT- Nest-PCR. RESULTS: The incidence of hypermethylation or homozygous deletion of AL L P16 gene was 80%, but no P16 gene was inactivated in the control group; homozygous deletion of P16 gene was higher in T-AL L than in hypermethylation; B- AL Hypermethylation in L is greater than homozygous deletion. MRNA expression was still found in 5 cases of hypermethylation of P16 gene, and no expression was found in the rest. Conclusion : Abnormality of P16 gene is one of the main pathogenesis of AL L. Homozygous deletion of T-AL L P16 gene is the main expression, while the hypermethylation of B-AL L P16 is the main expression. At the same time, regardless of homozygous deletion or hypermethylation of P16 gene, it can highly inhibit the expression of m RNA.