title: Correlation between the proliferative response to granulocyte colony-stimulating factor and the positivity of transferrin receptor in acute myeloblastic leukemia cells.
abstract: The use of granulocyte colony-stimulating factor (G-CSF) after chemotherapy for acute myeloblastic leukemia (AML) has been reported. However, there is a drawback in that G-CSF may stimulate the proliferation of AML progenitors. To determine the parameter(s) indicative of responsiveness of AML blasts to G-CSF, various surface phenotypes of blasts were examined in relation to the blast colony formation stimulated by G-CSF in 39 AML patients. A correlation was found only with transferrin receptor positivity among the various phenotypes studied. The population mean of percentages of transferrin receptor-positive blasts in the group responding to G-CSF in vitro was significantly higher than that of blasts in the group not responding to G-CSF. A further correlation was found between transferrin receptor positivity and the number of G-CSF receptors on the blasts; that is, blasts expressing more G-CSF receptors have greater transferrin receptor positivity. In our previous study, we observed that blasts with a large number of G-CSF receptors produce more colonies in response to G-CSF. These results indicated that blasts expressing more transferrin receptors have a larger number of G-CSF receptors and may show more active proliferation in response to G-CSF. Therefore, the proliferative response of blasts to G-CSF can be predicted by examining transferrin receptor positivity. The clinical use of G-CSF in AML patients may be recommended when the patient's blasts have a low level of transferrin receptor expression. The measurement of transferrin receptors on blasts, instead of the rather complicated G-CSF receptor determination, would be a useful indicator for the safer application of G-CSF in AML patients.
authors.affiliation: Department of Medicine, Tokyo Women's Medical College, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Motoji
authors.forename: M
authors.initials: M
authors.lastname: Mineshima
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: M
authors.initials: M
authors.lastname: Takanashi
authors.forename: M
authors.initials: M
authors.lastname: Masuda
authors.forename: K
authors.initials: K
authors.lastname: Oshimi
authors.forename: H
authors.initials: H
authors.lastname: Mizoguchi
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D000954:Antigens, Surface / Q000032:analysis; D001853:Bone Marrow / Q000473:pathology*; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D016179:Granulocyte Colony-Stimulating Factor / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000097:blood / Q000378:metabolism / Q000473:pathology*; D016188:Receptors, Granulocyte Colony-Stimulating Factor / Q000032:analysis; D011990:Receptors, Transferrin / Q000032:analysis*; D011994:Recombinant Proteins / Q000378:metabolism / Q000494:pharmacology
chemical_list: D015703:Antigens, CD; D000954:Antigens, Surface; D016188:Receptors, Granulocyte Colony-Stimulating Factor; D011990:Receptors, Transferrin; D011994:Recombinant Proteins; D016179:Granulocyte Colony-Stimulating Factor