Reduced expression of adhesion molecules and cell signaling receptors by chronic lymphocytic leukemia cells with 11q deletion.
作者： Sabine Sembries , Heike Pahl , Stephan Stilgenbauer , Hartmut Döhner , Folke Schriever
关键词: Cancer research 、 Integrin 、 Cell signaling 、 Receptor 、 Biology 、 Signal transduction 、 CD58 、 Complement receptor 1 、 CD48 、 Cell adhesion molecule
摘要: Deletions in chromosome bands 11q22-q23 were recently shown to be one of the most frequent aberrations 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 functional characteristics cells that may help explain pathophysiology this entity yet unknown. In present study, (n = 19) without analyzed for their expression functionally relevant cell surface molecules 57). carried significantly lower levels adhesion CD11a/CD18 (integrin L/β2), CD11c/CD18 X/β2), CD31 (PECAM-1), CD48, CD58 (LFA-3). Furthermore, expressed less signaling receptors CD45 (leukocyte common antigen [LCA]), CD6, CD35 (complement receptor 1), CD39. Reduced low-level CD49d correlated decreased overall survival. or did not differ growth fractions, transcription factor NF-κB, response mitogenic stimuli. Decreased contribute pathogenesis subgroup deletion.
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