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Prepublished online as a Blood First Edition Paper on July 18, 2002; DOI 10.1182/blood-2002-01-0222.
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Blood, 1 December 2002, Vol. 100, No. 12, pp. 3887-3896
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Clinical significance of phenotypic features of blasts in
patients with myelodysplastic syndrome
Kiyoyuki Ogata,
Kyoko Nakamura,
Norio Yokose,
Hideto Tamura,
Mikiko Tachibana,
Osamu Taniguchi,
Rika Iwakiri,
Tatsuyuki Hayashi,
Hisashi Sakamaki,
Yoshiro Murai,
Kaoru Tohyama,
Shigeru Tomoyasu,
Yasunobu Nonaka,
Mayumi Mori,
Kazuo Dan, and
Yataro Yoshida
From the Division of Hematology, Nippon Medical School,
Hematonosis Cell Analysis Center, Otsuka Assay Laboratories,
Division of Hematology, Tokyo Metropolitan Geriatric Hospital, Division
of Hematology, Tokyo Metropolitan Police Hospital, Division of
Hematology, Tokyo Metropolitan Komagome Hospital, Division of
Hematology, Tokyo Metropolitan Tama Geriatric Hospital, Division of
Hematology, Showa University, Tokyo, Japan; Division of Hematology,
Kyoto University, and Division of Hematology, Takeda Hospital, Kyoto,
Japan.
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.
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