Objective:To report 4 cases of biphenotypic acute leukemia(BAL)with t(8;21)(q22;q22),and analyze the characteristics of morphology,immune phenotype,chromosome karyotype(MIC)and clinical manifestations.Methods:The BAL ...Objective:To report 4 cases of biphenotypic acute leukemia(BAL)with t(8;21)(q22;q22),and analyze the characteristics of morphology,immune phenotype,chromosome karyotype(MIC)and clinical manifestations.Methods:The BAL patients with t(8;21)(q22;q22)(group A)were compared with the randomly selected BAL patients with other clonical chromo- somal changes(group B)and acute myeloid leukemia M2 cases with t(8;21)(q22;q22)(group C)in MIC and clinical features. Results:BAL with t(8;21)(q22;q22)showed acute myeloid leukemia with high percentages of blast cells morphologically; revealed co-positive to B-lymphoid and myeloid lineages,frequent and high expressions of CD34 and CD33;were responsive to chemotherapy for myeloid and lymphocytic leukemia simultaneously well.Conclusion:A new subset of BAL with t(8;21)(q22;q22)was reported,and this suggests that the leukemia colony with t(8;21)(q22;q22)might originate from early phase of hematopoiesis.展开更多
AIM: To analyze loss of heterozygosity (LOH) and homozygous deletion on p53 gene (exon2-3, 4 and 11), chromosome 10q22-10q23 and 22q11.2 -22q12.1 in human hepatocellular carcinoma (HCC).METHODS: PCR and PCR-based micr...AIM: To analyze loss of heterozygosity (LOH) and homozygous deletion on p53 gene (exon2-3, 4 and 11), chromosome 10q22-10q23 and 22q11.2 -22q12.1 in human hepatocellular carcinoma (HCC).METHODS: PCR and PCR-based microsatellite polymorphism analysis techniques were used.RESULTS: LOH was observed at D10S579 (10q22-10q23) in 4 of 20 tumors (20%), at D22S421 (22q11.2-22q12.1) in 3 of 20(15%), at TP53.A (p53gene exon 2-3) in 4 of 20 (20%), at TP53.B (p53gene exon 4) in 6 of 20(30%), and at TP53.G (p53gene exon 11)in 0 of 20(0%). Homozygous deletion was detected at 10q22-10q23(8/20; 40%), 22q11.2-22q12.1(8/20; 40%), p53 gene exon 2-3(0/20;0%), p53gene exon 4(6/20; 30%), and p53gene exon 11(2/20; 10%).CONCLUSION: There might be unidentified tumor suppressor genes on chromosome 10q22-10q23 and 22q11.2-22q12.1 that contribute to the pathogenesis and development of HCC.展开更多
基金in part by the Natural Science Fund of Jiangsu Province(2004BK424)the 135 Key Department Fund of Jiangsu Province(135XY0416)the Outstanding Person Fund of First Affiliated Hospital of Soochow University(2004YQG05).
文摘Objective:To report 4 cases of biphenotypic acute leukemia(BAL)with t(8;21)(q22;q22),and analyze the characteristics of morphology,immune phenotype,chromosome karyotype(MIC)and clinical manifestations.Methods:The BAL patients with t(8;21)(q22;q22)(group A)were compared with the randomly selected BAL patients with other clonical chromo- somal changes(group B)and acute myeloid leukemia M2 cases with t(8;21)(q22;q22)(group C)in MIC and clinical features. Results:BAL with t(8;21)(q22;q22)showed acute myeloid leukemia with high percentages of blast cells morphologically; revealed co-positive to B-lymphoid and myeloid lineages,frequent and high expressions of CD34 and CD33;were responsive to chemotherapy for myeloid and lymphocytic leukemia simultaneously well.Conclusion:A new subset of BAL with t(8;21)(q22;q22)was reported,and this suggests that the leukemia colony with t(8;21)(q22;q22)might originate from early phase of hematopoiesis.
基金Supported by the Natural Science Foundation of Anhui Province,No.99044312(YW),No.01043716(SYG)and Natural Science Foundation of Anhui Educational Commission,No.JL-97-077(YW)
文摘AIM: To analyze loss of heterozygosity (LOH) and homozygous deletion on p53 gene (exon2-3, 4 and 11), chromosome 10q22-10q23 and 22q11.2 -22q12.1 in human hepatocellular carcinoma (HCC).METHODS: PCR and PCR-based microsatellite polymorphism analysis techniques were used.RESULTS: LOH was observed at D10S579 (10q22-10q23) in 4 of 20 tumors (20%), at D22S421 (22q11.2-22q12.1) in 3 of 20(15%), at TP53.A (p53gene exon 2-3) in 4 of 20 (20%), at TP53.B (p53gene exon 4) in 6 of 20(30%), and at TP53.G (p53gene exon 11)in 0 of 20(0%). Homozygous deletion was detected at 10q22-10q23(8/20; 40%), 22q11.2-22q12.1(8/20; 40%), p53 gene exon 2-3(0/20;0%), p53gene exon 4(6/20; 30%), and p53gene exon 11(2/20; 10%).CONCLUSION: There might be unidentified tumor suppressor genes on chromosome 10q22-10q23 and 22q11.2-22q12.1 that contribute to the pathogenesis and development of HCC.
