Reduced expression of adhesion molecules and cell signaling receptors by chronic lymphocytic leukemia cells with 11q deletion

被引:48
作者
Sembries, S
Pahl, H
Stilgenbauer, S
Döhner, H
Schriever, F
机构
[1] Humboldt Univ, Univ Hosp Rudolf Virchow, Med Klin, Dept Hematol & Oncol, D-13353 Berlin, Germany
[2] Univ Freiburg, Inst Expt Anaesthesiol, Freiburg, Germany
[3] Heidelberg Univ, Med Klin & Poliklin 5, Heidelberg, Germany
关键词
D O I
10.1182/blood.V93.2.624.402k10_624_631
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. (C) 1999 by The American Society of Hematology.
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页码:624 / 631
页数:8
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