title: Dyshematopoiesis in de novo acute myeloid leukemia: cell biological features and prognostic significance.
abstract: Dyshematopoiesis was found in 44 (42.3%) of 104 cases of de novo acute myeloid leukemia (AML). Dyshematopoietic AML (dys-AML) and AML without hematopoietic dysplasia (non-dys-AML) were compared with regard to biological, hematological, immunophenotypic, and cytogenetic parameters as well as prognostic criteria. Median age of patients was 55 years in both groups. In dys-AML, the median leukocyte count (p = 0.04), peripheral blast (p = 0.02) and medullary blast cell count (p < 0.001) were significantly decreased, whereas the median platelet count (p - 0.04) was increased. Immunophenotyping demonstrated that leukemic blast cells in dys-AML more frequently expressed the adhesion molcules CD54 (p = 0.05) and CD58 (p = 0.08) than leukemic cells in non-dys-AML. Cytogenetically, we distinguished two karyotypic patterns, one group with a normal karyotype or prognostically favorable single chromosome aberrations ("P(0)-karyotype"), and another one with unfavorable single aberrations or complex aberrations ("P(1)-karyotype"). The incidence of these groups was not significantly different between dys-AML and non-dys-AML. Complete remission rate (CRR) after induction chemotherapy (p = 0.03) and overall survival time (OS; p = 0.03) were significantly lower in dys-AML. In addition, median disease free survival (DFS; p = n.s.) was inferior compared to non-dys-AML. In the dys-AML as well as in the non-dys-AML patient group, CRR, DFS, and OS were decreased in the P(1)-compared to the P(0)-subgroup. We conclude that dyshematopoietic AML is characterized by specific cell biological features and that hematopoietic and cytogenetic status represent complementary prognostic factors in de novo AML.
authors.affiliation: Department of Hematology, Oncology and Clinical Immunology, Heinrich-Heine-University of Duesseldorf, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Meckenstock
authors.forename: C
authors.initials: C
authors.lastname: Aul
authors.forename: B
authors.initials: B
authors.lastname: Hildebrandt
authors.forename: A
authors.initials: A
authors.lastname: Heyll
authors.forename: U
authors.initials: U
authors.lastname: Germing
authors.forename: A
authors.initials: A
authors.lastname: Wehmeier
authors.forename: A
authors.initials: A
authors.lastname: Giagounidis
authors.forename: T
authors.initials: T
authors.lastname: Suedhoff
authors.forename: M
authors.initials: M
authors.lastname: Burk
authors.forename: D
authors.initials: D
authors.lastname: Soehngen
authors.forename: W
authors.initials: W
authors.lastname: Schneider
mesh_terms: D000208:Acute Disease; D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D001853:Bone Marrow / Q000473:pathology*; D002453:Cell Cycle; D004273:DNA, Neoplasm / Q000032:analysis; D018572:Disease-Free Survival; D005434:Flow Cytometry; D006410:Hematopoiesis; D006801:Humans; D016130:Immunophenotyping; D007621:Karyotyping; D007951:Leukemia, Myeloid / Q000235:genetics / Q000401:mortality / Q000473:pathology*; D015993:Life Tables; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000032:analysis; D014411:Neoplastic Stem Cells / Q000473:pathology*; D011379:Prognosis; D016019:Survival Analysis; D015996:Survival Rate
chemical_list: D015703:Antigens, CD; D004273:DNA, Neoplasm; D009363:Neoplasm Proteins