title: Phenotypical characteristics of acute myelocytic leukemia associated with the t(8;21)(q22;q22) chromosomal abnormality: frequent expression of immature B-cell antigen CD19 together with stem cell antigen CD34.
abstract: Twenty-three acute myelocytic leukemia (AML) patients with t(8;21) chromosomal abnormality, all classified as M2 (French-American-British [FAB] classification), were investigated. Blastic cells from all patients were positive for the stem cell-associated antigens, CD34 and HLA-DR, and the immature myeloid antigens, CD13 and CD33. The nonblastic leukemic cells expressed the more mature myeloid antigens, CD11b and CD15, with loss of the immature phenotype. The incidence of positivities for the stem cell-associated antigens, CD34 and HLA-DR, in t(8;21) AML cells was significantly higher in comparison with those in other AML showing granulocytic differentiation (M2 or M3). AML cells with t(8;21) also showed some phenotypic abnormalities. Frequent expression of CD19 was found in the blastic population of t(8;21) AML (18 of 23 cases) without other B-cell antigens and Ig gene rearrangements. CD19 expression was confirmed by immunocytochemistry and Northern blotting. The CD19+ blastic cells coexpressed both CD34 and HLA-DR. In addition, CD33+ cells among the blastic fraction in t(8;21) AML cells were fewer in number than in those of M2 or M3 AML without t(8;21). Our findings indicate that leukemic blasts of t(8;21) AML commonly express CD19 while preserving the stem cell-associated antigens, and differentiate into the granulocytic pathway with discordant maturation such as low CD33 expression.
authors.affiliation: Second Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kita
authors.forename: K
authors.initials: K
authors.lastname: Nakase
authors.forename: H
authors.initials: H
authors.lastname: Miwa
authors.forename: M
authors.initials: M
authors.lastname: Masuya
authors.forename: K
authors.initials: K
authors.lastname: Nishii
authors.forename: N
authors.initials: N
authors.lastname: Morita
authors.forename: N
authors.initials: N
authors.lastname: Takakura
authors.forename: A
authors.initials: A
authors.lastname: Otsuji
authors.forename: S
authors.initials: S
authors.lastname: Shirakawa
authors.forename: T
authors.initials: T
authors.lastname: Ueda
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis / Q000235:genetics*; D018941:Antigens, CD19; D018951:Antigens, CD20; D018952:Antigens, CD34; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis / Q000235:genetics*; D001402:B-Lymphocytes / Q000276:immunology*; D001483:Base Sequence; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D002891:Chromosomes, Human, Pair 21; D002898:Chromosomes, Human, Pair 8; D006801:Humans; D007621:Karyotyping; D015470:Leukemia, Myeloid, Acute / Q000235:genetics*; D008969:Molecular Sequence Data; D009838:Oligodeoxyribonucleotides; D010641:Phenotype; D016133:Polymerase Chain Reaction; D013234:Stem Cells / Q000276:immunology*; D014178:Translocation, Genetic
chemical_list: D015703:Antigens, CD; D018941:Antigens, CD19; D018951:Antigens, CD20; D018952:Antigens, CD34; D000944:Antigens, Differentiation, B-Lymphocyte; D009838:Oligodeoxyribonucleotides