急性白血病p16基因的研究(英文)

Study on p16 gene in acute leukemia

为研究p16抑癌基因在急性白血病中的变化,用ABC法研究了61例急性白血病细胞表面p16抗原的表达和用多重PCR法研究了51例急性白血病p16基因的结构缺陷。结果发现白血病患者p16抗原的表达明显低于正常人(P<0.001),其中急性淋巴细胞白血病(ALL)又明显低于急性髓细胞白血病(AML)(P<0.05);但在AML和ALL完全缓解组(CR)和未缓解组(NR),p16抗原表达均无差异(P>0.05)。在30例ALL中仅发现4例p16基因第二外显子纯合子缺失,在21例AML未发现pl6基因的结构变化,说明p16基因的表达缺陷是急性白血病发生和发展中的主要变化,而结构异常并不是其演变中的必需分子事件。

To study the change of suppressing cancer gene p16 in acute leukemia, the p16 antigen expression of leukemia cell surface in 61 cases with acute leukemia and gene structural defect in 51 cases with acute leukemia were investigated by ABC assay and multiple comparative PCR method, respectively. It was found that antigen expression of p16 in leukemia cells was obviously lower than that of in normal individuals ( P< 0.001). At the same time, antigen expression in ALL was lower than that in A ML (P<0.05). Compared with complete remission (CR) and non-remission (NR) in AML and ALL, respectively, there were no significant difference (P>0.05). The exon 2 of p16 gene showed homozygous deletion only in 4 cases from 30 cases with ALL. No structural defect was found in 21 cases with AML. It was demonstrated that expression defect of p16 gene was a main cause in development and evolution of acute leukemia while structural defect was not a necessary molecular event.