Abstract
Data concerning the presence and the functionality of Fas receptor in malignant B-cells are controversial. We have analyzed Fas molecules on B-cells from patients with B-chronic lymphocytic leukemia (B-CLL) cells. We observed a large variability, both of percentage of Fas-positive cells and of intensity of Fas level. Fas triggering was inefficient in inducing apoptosis whatever the number of Fas-positive B-cells, the amount of Fas receptors. B-cells were also resistant to etoposide treatment, but able to undergo apoptosis after dexamethasone treatment. We suggest that the Fas apoptotic pathway is altered in B-CLL patients at the initial step(s) of apoptotic machinery.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing*
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Adult
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Aged
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Aged, 80 and over
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Apoptosis / drug effects*
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Blotting, Western
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Carrier Proteins / genetics
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Carrier Proteins / physiology
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Caspases / metabolism
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Caspases / physiology
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Cell Survival / physiology
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Dexamethasone / pharmacology
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Drug Resistance, Neoplasm
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Etoposide / pharmacology
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Fas Ligand Protein
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Fas-Associated Death Domain Protein
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Female
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Flow Cytometry
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Humans
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Leukemia, Lymphocytic, Chronic, B-Cell / etiology
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Leukemia, Lymphocytic, Chronic, B-Cell / metabolism
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Leukemia, Lymphocytic, Chronic, B-Cell / pathology*
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Male
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / physiology
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Middle Aged
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RNA, Messenger / analysis
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction / drug effects
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fas Receptor / analysis
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fas Receptor / pharmacology
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fas Receptor / physiology*
Substances
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Adaptor Proteins, Signal Transducing
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Carrier Proteins
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FADD protein, human
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FASLG protein, human
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Fas Ligand Protein
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Fas-Associated Death Domain Protein
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Membrane Glycoproteins
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RNA, Messenger
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fas Receptor
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Etoposide
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Dexamethasone
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Caspases