Upstream Mediators of the Fas Apoptotic Transduction Pathway Are Defective in B-Chronic Lymphocytic Leukemia

Roué G (1) , Lancry L (1) , Duquesne F (1) , Salaün V (2) , Troussard X (2, 1) , Brigitte Sola (1)

1 Laboratoire de recherche Immunopathologie et infection
2 Laboratoire d'Hématologie Biologique [CHU Caen]

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.

Keywords: Fas (CD95/APO-1); Caspase; Apoptosis; Death receptor; Signal transduction; Resistance

Domains: Life Sciences [q-bio]

Roué G, Lancry L, Duquesne F, Salaün V, Troussard X, et al.. Upstream Mediators of the Fas Apoptotic Transduction Pathway Are Defective in B-Chronic Lymphocytic Leukemia. Leukemia Research, 2001, 25 (11), pp.967-980. ⟨10.1016/s0145-2126(01)00063-7⟩. ⟨hal-01762038⟩