title: Decreased L-selectin expression in CD34-positive cells from patients with chronic myelocytic leukaemia.
abstract: Abnormal adhesive interaction between bone marrow stroma and progenitors, one of the causes of unregulated proliferation in chronic myelocytic leukaemia (CML), may be caused by some alterations in adhesion molecules on CML progenitors. We investigated the expression of adhesion molecules (CD44, VLA-5, VLA-4, LFA-1, ICAM-1, L-selectin and c-kit) on bone marrow CD34++ cells from 16 CML patients by three-colour flow cytometry. The mean percentage of cells expressing L-selectin in the CD34++CD38+(or)++ fraction from untreated CML patients was significantly lower, and that in the CD34++CD38- fraction tended to be lower than that from normal controls. Among 11 CML patients treated with interferon-alpha (IFN-alpha), the mean percentage of the cells expressing L-selectin in the CD34++CD38- fraction from three patients with a low percentage of Ph1(+) cells in bone marrow was significantly higher than that from five patients with a high percentage of Ph1(+) cells. In addition, L-selectin expression rate was inversely correlated to the percentage of Ph1(+) cells. There was no significant difference between the untreated patients and normal controls with regard to the expression rates of the other adhesion molecules in each CD34++ fraction except LFA-1. These data suggest that decreased L-selectin expression in CML CD34++ cells reflects one of the features of malignant CML progenitors.
authors.affiliation: Department of Environment and Mutation, Research Institute for Radiation Biology and Medicine, Hiroshima University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kawaishi
authors.forename: A
authors.initials: A
authors.lastname: Kimura
authors.forename: O
authors.initials: O
authors.lastname: Katoh
authors.forename: A
authors.initials: A
authors.lastname: Sasaki
authors.forename: N
authors.initials: N
authors.lastname: Oguma
authors.forename: A
authors.initials: A
authors.lastname: Ihara
authors.forename: Y
authors.initials: Y
authors.lastname: Satow
mesh_terms: D036541:ADP-ribosyl Cyclase; D051997:ADP-ribosyl Cyclase 1; D000328:Adult; D000368:Aged; D015703:Antigens, CD; D018952:Antigens, CD34 / Q000032:analysis*; D000943:Antigens, Differentiation / Q000378:metabolism; D003116:Color; D005434:Flow Cytometry; D006412:Hematopoietic Stem Cells / Q000378:metabolism*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016898:Interferon-alpha / Q000627:therapeutic use; D019041:L-Selectin / Q000378:metabolism*; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000378:metabolism* / Q000628:therapy; D008562:Membrane Glycoproteins; D008875:Middle Aged; D009699:N-Glycosyl Hydrolases / Q000378:metabolism; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D016029:Receptors, Very Late Antigen / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D018952:Antigens, CD34; D000943:Antigens, Differentiation; D016898:Interferon-alpha; D008562:Membrane Glycoproteins; D016029:Receptors, Very Late Antigen; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin; D019009:Proto-Oncogene Proteins c-kit; D009699:N-Glycosyl Hydrolases; D036541:ADP-ribosyl Cyclase; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1