Defects in signal transduction pathways in chronic B lymphocytic leukemia cells

Leukemia & Lymphoma
S A JabbarR G Wickremasinghe

Abstract

B chronic lymphocytic leukemia (B-CLL) and hairy cell leukemia (HCL) cells are refractory to many of the signals which activate normal B cells but are stimulated to proliferate by tumor necrosis factor (TNF). Cell signalling by TNF is mediated in part by the induction of the transcription factor families AP-1 and NF-kappa B. In some cellular contexts, these factors play a role in regulating cell cycle transit. AP-1 binds DNA as dimers of jun and fos family proteins and is regulated by a cascade of protein kinases which eventually activate a mitogen-activated protein kinase (MAP kinase) and also by protein kinase C. Three pathways have been implicated in the activation of NF-kappa B by extracellular ligands. 1, the activation of protein kinase C by diacylglycerol generated by ligand-mediated activation of phosphatidylcholine hydrolysis, 2, stimulation of specific protein kinases by ceramide generated following activation of a sphingomyelinase by diacylglycerol and 3, a novel pathway involving ligand-induced generation of free radical species. In B-CLL and HCL cells, the generation of nuclear-localized c-jun and c-fos proteins (components of AP-1) in response to TNF or PMA appears to be blocked. Whereas PMA failed to induce NF-ka...Continue Reading

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Citations

May 10, 2003·Blood Cells, Molecules & Diseases·George B SegelNancy Wang
Jul 14, 2010·Best Practice & Research. Clinical Haematology·Erin Hertlein, John C Byrd
Sep 3, 2010·Cytometry. Part B, Clinical Cytometry·Emel Eksioglu-DemiralpMahmut Bayik
Feb 3, 2000·Critical Reviews in Clinical Laboratory Sciences·G LiuR L Hébert
Jan 14, 1999·The American Journal of Physiology·J BinkoH Majewski

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