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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。
In order to study the changes of p16 tumor suppressor gene in acute leukemia, the expression of p16 antigen on the surface of 61 acute leukemia cells was studied by ABC method and the structural defects of 51 acute leukemia p16 genes were studied by multiplex PCR. The results showed that the expression of p16 antigen in leukemia patients was significantly lower than normal (P<0.001), and acute lymphoblastic leukemia (ALL) was significantly lower than that of acute myeloid leukemia (AML) (P<0.05); however, it was completely in AML and ALL. There was no difference in p16 antigen expression between the remission group (CR) and the non-remission group (NR) (P>0.05). Only 4 cases of p16 gene exon homozygote deletion were found in 30 cases of ALL, and no structural changes in pl6 gene were found in 21 cases of AML, indicating that p16 gene expression deficiency is the major change in the occurrence and development of acute leukemia. Structural anomalies are not essential molecular events in their evolution.