title: CD34+CD7+ leukemic progenitor cells may be involved in maintenance and clonal evolution of chronic myeloid leukemia.
abstract: OBJECTIVE
  We analyzed CD34+ cells coexpressing CD7 in chronic myeloid leukemia (CML) in chronic phase (CP) or accelerated phase (AP) to clarify their role in progression or regression of the disease during treatment.
  
  
  METHODS
  Enumeration of CD34+CD7+ cells was done on bone marrow nucleated cells from normal donors and CML patients. Fluorescence in situ hybridization analysis was done on sorted CD34+CD7+and CD34+CD7- cells to examine the occupancy rate of each fraction by BCR-ABL+ cells with or without additional cytogenetic abnormalities.
  
  
  RESULTS
  The proportion of CD34+CD7+cells was significantly affected by the treatment outcome and/or the disease status as follows: 20.5 +/- 10.4% in normal donors (n = 22), 18.1 +/- 10.2% in CP with major cytogenetic response (n = 14), 53.0 +/- 12.9% in CP at diagnosis (n = 18), 55.0 +/- 15.8% in CP with minor or no cytogenetic response (n = 28), and 70.2 +/- 18.1% in AP (n = 6). The proportion of CD34+CD7+cells decreased in parallel with cytogenetic improvement in individual patients. In six untreated CP patients, the ratio of BCR-ABL+ cells was comparable between each fraction. In three patients with major cytogenetic response, the ratio of BCR-ABL+ cells was remarkably lower in CD34+CD7- cells than in CD34+CD7+cells. In three AP patients with additional cytogenetic abnormalities, extra signals were detected at a much higher rate in CD34+CD7+ cells than in CD34+CD7- cells.
  
  
  CONCLUSIONS
  Our results suggest that CD34+CD7+ cells may be involved in maintenance and clonal evolution of BCR-ABL+ cells in CML.
authors.affiliation: Department of Haematology/Oncology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato, Tokyo 108-8639, Japan.
authors.forename: Nobuharu
authors.initials: N
authors.lastname: Kosugi
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Ebihara
authors.forename: Tatsutoshi
authors.initials: T
authors.lastname: Nakahata
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Saisho
authors.forename: Shigetaka
authors.initials: S
authors.lastname: Asano
authors.forename: Arinobu
authors.initials: A
authors.lastname: Tojo
mesh_terms: D000293:Adolescent; D000328:Adult; D018952:Antigens, CD34 / Q000235:genetics / Q000378:metabolism*; D019011:Antigens, CD7 / Q000235:genetics / Q000378:metabolism*; D001853:Bone Marrow; D002869:Chromosome Aberrations; D002999:Clone Cells; D020732:Cytogenetic Analysis; D018450:Disease Progression; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000378:metabolism; D006412:Hematopoietic Stem Cells / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D014019:Tissue Donors
chemical_list: D018952:Antigens, CD34; D019011:Antigens, CD7; D016044:Fusion Proteins, bcr-abl