title: Clinical significance of phenotypic features of blasts in patients with myelodysplastic syndrome.
abstract: Knowledge of the blast phenotype in myelodysplastic syndrome (MDS) would be valuable, as in other malignancies, but remains sparse. This is mainly because MDS blasts are a minor population in clinical samples, making analysis difficult. Thus, for this blast phenotype study, we prepared blast-rich specimens (using a new density centrifugation reagent for harvesting blasts) from blood and marrow samples of 95 patients with various MDS subtypes and 21 patients with acute leukemia transformed from MDS (AL-MDS). Flow cytometry revealed that a high proportion of the enriched blast cells (EBCs) from almost all patients showed an immunophenotype of committed myeloid precursors (CD34(+)CD38(+)HLA-DR(+)CD13(+)CD33(+)), regardless of the disease subtype. The cytochemical reaction for myeloperoxidase was negative in 58% of the cases. Thus, the EBC phenotype is more immature in MDS than in de novo acute myeloid leukemia. MDS EBCs often coexpressed stem cell antigens and late-stage myeloid antigens asynchronously, but rarely expressed T- and B-lymphoid cell-specific antigens. Markers for myeloid cell maturation (CD10 and CD15) were more prevalent on EBCs from low-risk MDS (refractory anemia [RA] and RA with ringed sideroblasts), whereas markers for myeloid cell immaturity (CD7 and CD117) were more prevalent on EBCs from high-risk MDS (chronic myelomonocytic leukemia, RA with excess blasts [RAEB], and RAEB in transformation) and AL-MDS. A shift to a more immature phenotype of EBCs, accompanying disease progression, was also documented by sequential phenotyping of the same patients. Further, CD7 positivity of EBCs was an independent variable for a poor prognosis in MDS. These data represent new, valuable information regarding MDS.
authors.affiliation: Division of Hematology, Nippon Medical School, Kyoto, Japan. ogata@nms.ac.jp
authors.forename: Kiyoyuki
authors.initials: K
authors.lastname: Ogata
authors.forename: Kyoko
authors.initials: K
authors.lastname: Nakamura
authors.forename: Norio
authors.initials: N
authors.lastname: Yokose
authors.forename: Hideto
authors.initials: H
authors.lastname: Tamura
authors.forename: Mikiko
authors.initials: M
authors.lastname: Tachibana
authors.forename: Osamu
authors.initials: O
authors.lastname: Taniguchi
authors.forename: Rika
authors.initials: R
authors.lastname: Iwakiri
authors.forename: Tatsuyuki
authors.initials: T
authors.lastname: Hayashi
authors.forename: Hisashi
authors.initials: H
authors.lastname: Sakamaki
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Murai
authors.forename: Kaoru
authors.initials: K
authors.lastname: Tohyama
authors.forename: Shigeru
authors.initials: S
authors.lastname: Tomoyasu
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Nonaka
authors.forename: Mayumi
authors.initials: M
authors.lastname: Mori
authors.forename: Kazuo
authors.initials: K
authors.lastname: Dan
authors.forename: Yataro
authors.initials: Y
authors.lastname: Yoshida
mesh_terms: D000208:Acute Disease; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D016022:Case-Control Studies; D002469:Cell Separation / Q000379:methods; D002499:Centrifugation, Density Gradient / Q000379:methods; D018450:Disease Progression; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016130:Immunophenotyping; D007938:Leukemia / Q000235:genetics / Q000473:pathology; D008297:Male; D008793:Metrizamide; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000235:genetics / Q000473:pathology*; D010641:Phenotype; D011379:Prognosis; D016019:Survival Analysis
chemical_list: D015703:Antigens, CD; D008793:Metrizamide