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

Citation
S. Sembries et al., Reduced expression of adhesion molecules and cell signaling receptors by chronic lymphocytic leukemia cells with 11q deletion, BLOOD, 93(2), 1999, pp. 624-631
Citations number
43
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
BLOOD
ISSN journal
00064971 → ACNP
Volume
93
Issue
2
Year of publication
1999
Pages
624 - 631
Database
ISI
SICI code
0006-4971(19990115)93:2<624:REOAMA>2.0.ZU;2-V
Abstract
Deletions in chromosome bands 11q22-q23 were recently shown to be one of th e most frequent chromosome aberrations in B-cell chronic lymphocytic leukem ia (B-CLL). Patients suffering from B-CLL with 11q deletion are characteriz ed by extensive lymphadenopathy, rapid disease progression, and short survi val times. Phenotypic and functional characteristics of B-CLL cells with 11 q 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 rele vant 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), CD 48, and CD58 (LFA-3). Furthermore, B-CLL cells with 11q deletion expressed less the cell signaling receptors CD45 (leukocyte common antigen [LCA]), CD 6, CD35 (complement receptor 1), and CD39. Reduced CD45 levels and low-leve l expression of CD49d correlated with decreased overall survival. B-CLL cel ls with or without 11q deletion did not differ in their growth fractions, e xpression levels of transcription factor NF-kappa B, or their response to m itogenic stimuli. Decreased levels of functionally relevant adhesion molecu les and of cell signaling receptors may contribute to the pathogenesis of t he subgroup of B-CLL characterized by 11q22-q23 deletion. (C) 1999 by The A merican Society of Hematology.