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Imatinib restores expression of CD62L in BCR‐ABL‐positive cells
Author(s) -
Fruehauf S.,
Topaly J.,
Schad M.,
Paschka P.,
Gschaidmeier H.,
Zeller W. J.,
Hochhaus A.,
Ho A. D.
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1002507
Subject(s) - imatinib , chronic myelogenous leukemia , biology , cancer research , tyrosine kinase , abl , flow cytometry , k562 cells , leukemia , imatinib mesylate , bone marrow , breakpoint cluster region , microbiology and biotechnology , immunology , signal transduction , myeloid leukemia , receptor , biochemistry
Chronic myelogenous leukemia (CML) is characterized by aberrant trafficking of malignant hematopoietic progenitor cells in the peripheral blood. Expression of the cell adhesion molecule CD62L was reported to be significantly lower in CML patients than in normal controls. We studied whether the transcription of CD62L in CML cells is dependent on the activity of the BCR‐ABL tyrosine kinase. Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR‐ABL‐positive cell lines (BV173, SD‐1), we observed a dose‐dependent increase in CD62L RNA levels of up to 45‐fold by a quantitative, real‐time polymerase chain reaction and an increase in the amount of cell surface‐bound CD62L of up to 18‐fold by quantitative flow cytometry, respectively. These data are validated by an increased CD62L expression in the bone marrow of patients (n=6) with advanced CML who received imatinib. Restoration of defective cell adhesion mediated via the CD62L pathway may be one mechanism of action of imatinib in BCR‐ABL‐positive leukemias.