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Immunophenotype of c‐kit cells in normal human bone marrow: implications for the detection of minimal residual disease in AML
Author(s) -
Macedo A.,
Orfao A.,
Martianez A.,
Vidriales M. B.,
Valverde B.,
LoapezBerges M. C.,
Miguel J. F. San
Publication year - 1995
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1995.tb03309.x
Subject(s) - cd117 , cd34 , cd33 , cd15 , immunophenotyping , bone marrow , myeloid , antigen , minimal residual disease , immunology , medicine , microbiology and biotechnology , pathology , biology , stem cell
Summary. In the present study, seven normal human bone marrow samples from healthy volunteers have been analysed in order to investigate the immunophenotypic characteristics of the normal CD117 + cells and their utility for the detection of minimal residual disease in 71 acute myeloid leukaemia patients. Our results show that most of normal BM CD117 + cells coexpress the HLADR and the myeloid associated CD33 antigen. In addition, almost half of CD117 + cells are CD34 + , these cells displaying a different FSC/SSC distribution when compared to the CD117 + /CD34 − cells. No CD117 + /CD15 + and CD117 + /CD10 + cells were detected and very few CD117 + cells (<1 × 10 −3 ) expressing the HLADR − /CD34 − , CD33 + /HLADR − and CD34 + /HLADR − phenotypes were found to be present in normal BM. In contrast, from the 71 AML patients analysed, 34 had CD117 + /CD15 + blast cells and eight had the CD117 + phenotypes detected at low frequencies (<1 × 10 −3 ) in normal BM. In summary, the present study shows that the use of the CD117 antigen in different monoclonal antibodies combinations may be of great help for the detection of minimal residual disease in a high proportion of AML cases, especially in those patients displaying the CD117 + /CD15 + phenotype, because cells coexpressing both antigens in normal BM, if present, are at very low frequencies.