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Evidence for expression of early myeloid antigens in mature, non‐blast myeloid cells in myelodysplasia
Author(s) -
Xu Dongsheng,
Schultz Cynthia,
Akker Yelena,
Cannizzaro Linda,
Ramesh K.H.,
Du Juan,
Ratech Howard
Publication year - 2003
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.10372
Subject(s) - myelodysplastic syndromes , cd34 , myeloid , bone marrow , biology , myeloid leukemia , cytogenetics , haematopoiesis , karyotype , pathology , antigen , flow cytometry , stem cell , medicine , immunology , cancer research , genetics , chromosome , gene
Myelodysplastic syndromes (MDS) are clonal hematopoietic stem cell disorders with frequent cytogenetic abnormalities. They can arise de novo or be related to therapy. Although blasts in MDS have been studied extensively, there is little information available on the mature, non‐blast myeloid cells (NBMCs). We used a retrospective case‐control study design. NBMC populations in MDS (48 cases) and in tumor‐free control (12 cases) bone marrow samples were analyzed using multiparameter flow cytometry for mean side scatter (SSC) channel number and for expression of aberrant cell surface antigens. MDS cases were stratified on the basis of cytogenetic abnormalities. We report that NBMCs in MDS with normal karyotype expressed significantly higher HLA‐DR than controls ( P = 0.034). NBMCs in MDS cases with cytogenetic abnormalities and with ≥5% marrow blasts, compared with controls, had significantly higher CD34 and higher HLA‐DR but lower CD10 and lower SSC mean channel number. CD34 expression in NBMCs was significantly greater in therapy‐related MDS compared with de novo MDS ( P = 0.01), although the presence of cytogenetic abnormalities was not different ( P > 0.05). These data suggest that bone marrow, mature, NBMCs have phenotypic changes in MDS that are not seen in normal controls. Am. J. Hematol. 74:9–16, 2003. © 2003 Wiley‐Liss, Inc.