| objective: The mismatch repair genes play a role in maintaining the genetic stability of DNA . They are responsible for correcting mismatch basepairs that arise as a result of misincoporation errors during DNA replication. Deficient of MMR had been observed in tumors of hereditary nonpolyposis colon cancer (HNPCC) patients and several sporadic tumors. It had been observed in leukemia. It is prompted that deficient of MMR can also lead to hematological cell malignant proliferation. hMSH2 is one of the genes involved in human DNA mismatch repair .It was found to be capable of binding to mismatched nucleotides , proceeding the mismatch repair process . Loss of this function may lead to a mutator phenotype, which has been proposed to lead to the accumulation of the mutations in oncogenes or tumor-suppressor genes, it is one of the most frequently mutated genes in human cancers.p53 is another gene critical to the DNA repair process. The function of the p53 protein is to bind DNA and to regulate genes that control growth arrest and apoptosis. The p53 gene mutations had been reported in leukemia. For several years the immunologic identification of the p53 protein in human tumors has been considered a marker of p53 gene mutation. Some experiments found a high incidence of abnormal expression of MSH2 that was associated with p53 mutations. In order to investigate the mechanism of leukemic cell malignant proliferation the expression of hMSH2 and P53 in bone marrow cells of denovo acute leukemia will be determined by in situ hybridization and immunocytochemical methods.Materials and methods: (1) Subjects were divided into three groups: (1). The de novo acute lymphocytic leukemia (ALL) group (n=26, Male 15,Female 11,Mean age 28y); (2). The de novo acute myelogenous leukemia(AML) group (n=37, Male 24,Female 13,Mean age 37y), it included Ml 4 cases, M2 18 cases, M3 5 cases, M4 7 cases, M5 3 cases; according to the diagnostic standard worked out by FAB in 1986;<3). The control group (n=25, Male 12,Female 13,Mean age 35y). (2)Collecting the mononuclear cells of bone marrow of all subjects, testing the positive percentage of hMSH2 by in situ hybridization and the positive percentage of mtP53 protein expression by immunocytochemical method.(Count 500 cells and the positive cell to gain the percent) (3) The results were analyzed with chi-square test, simple correlation by SPSS10.0, and we established the standard of statistic significance as a =0.05 . result: (1) The positive cell percentage of hMSH2 mRNA expression in these three groups decreased gradually. They are (64.22 +8.51)% in the de novo ALL group, (53.98 + 9.69)% in the de novo AML group and (32.88+11.46)% in the control group, there are significant differences among three groups (P<0.05), as well as between each two groups (P<0.05). (2)The positive cell percentage of mtP53 protein expression in these three groups increased gradually. They are (12.63+6.66)% in the de novo ALL group, (21.50+7.72) % in the de novo AML group and (29.25+9.45) % in the control group. There are significant differences among three groups (P<0.05), as well as between each two groups (P<0.05). (3) The positive percentage of hMSH2 mRNA expression is significant higher in older age (+55) AML group (46.97 + 7.21) % than that in younger age (-55)AML group (58.25 + 8.51) % (P<0.05). The positive percentage of hMSH2 mRNA expression in old age (+55) ALL group(n=4), young age (-55)ALL group (n=22) are (38.4 + 8.17) % (31.88+11.83) %. There isn't significant difference between them (P>0.05). (4)The positive percentage of mtP53 protein expression in old age (+55) AML group, young age (-55)AML group are (18.75 + 8.16) % (22.81 + 7.29) %. There isn't significant difference between them (P<0.05). The positive percentage of mtP53 protein expression in old age (+55) ALL group,young age (-55)ALL group are (26.74+6.70)%, (30.07 + 9.76) %. There isn't significant difference between them (P>0.05). (5) There was a significant negative simple correlation between the positive perce...
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