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Blood, Vol. 93 No. 2 (January 15), 1999: pp. 624-631

Reduced Expression of Adhesion Molecules and Cell Signaling Receptors by Chronic Lymphocytic Leukemia Cells With 11q Deletion

Sabine Sembries, Heike Pahl, Stephan Stilgenbauer, Hartmut Döhner, and Folke Schriever

From the Medizinische Klinik, mit Schwerpunkt Hämatologie und Onkologie, Charité, Campus Virchow-Klinikum, Humboldt Universität, Berlin, Germany; Institut für Experimentelle Anaesthesiologie, Klinikum der Albert-Ludwigs-Universität, Freiburg, Germany; and Medizinische Klinik und Poliklinik V, Ruprecht-Karls-Universität, Heidelberg, Germany.

Deletions in chromosome bands 11q22-q23 were recently shown to be one of the most frequent chromosome aberrations in B-cell chronic lymphocytic leukemia (B-CLL). Patients suffering from B-CLL with 11q deletion are characterized by extensive lymphadenopathy, rapid disease progression, and short survival times. Phenotypic and functional characteristics of B-CLL cells with 11q deletion that may help to explain the pathophysiology of this entity are yet unknown. In the present study, B-CLL cells with (n = 19) and without (n = 19) 11q deletion were analyzed for their expression of functionally relevant cell surface molecules (n = 57). B-CLL cells with 11q deletion carried significantly lower levels of the adhesion molecules CD11a/CD18 (integrin alpha L/beta 2), CD11c/CD18 (integrin alpha X/beta 2), CD31 (PECAM-1), CD48, and CD58 (LFA-3). Furthermore, B-CLL cells with 11q deletion expressed less the cell signaling receptors CD45 (leukocyte common antigen [LCA]), CD6, CD35 (complement receptor 1), and CD39. Reduced CD45 levels and low-level expression of CD49d correlated with decreased overall survival. B-CLL cells with or without 11q deletion did not differ in their growth fractions, expression levels of transcription factor NF-kappa B, or their response to mitogenic stimuli. Decreased levels of functionally relevant adhesion molecules and of cell signaling receptors may contribute to the pathogenesis of the subgroup of B-CLL characterized by 11q22-q23 deletion.


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