1,721,013 research outputs found
Long-Term Effects of Rituximab in Rheumatoid Arthritis Clinical, Biologic, and Pharmacogenetic Aspects
Acute promyelocytic leucemia: low expression of multidrug resistance phenotype at onset suggest a favourable effect of gentuzumab ozogamicyn (CMA-676
A randomized, controlled, multicenter phase III study of the efficacy and safety of rituximab (rtx) monotherapy versus the best available treatment (bat) in patients with mixed cryoglobulinemia syndrome (MC)
Amifostine does not inhibit the toxic effects of anthracycline derivates or mitoxantrone on MDR tumor cell lines.
DC1 AND DC2 DETECTION IN BONE MARROW AND G-CSF PRIMED PB HARVEST FROM ALLOGENEIC STEM CELL DONORS
P-glycoprotein (PGP), lung resistance-related protein (LRP) and multidrug resistance-associated protein (MRP) expression in acute promyelocytic leukaemia
Flow cytometry evaluation of plasma cells contaminating leukapheresis pre- and post- CD34-positive selection-
Biological and clinical features of T-biphenotypic acute leukaemia: report from a single centre
Aberrant expression of TRAIL in B chronic lymphocytic leukemia (B-CLL) cells.
Analysis of peripheral blood (>85% CD19+/CD5+ B) lymphocytes, obtained from 44 patients affected by B chronic lymphoid leukemia (B-CLL), showed that surface TNF-related apoptosis inducing ligand (TRAIL) was expressed in all samples and at higher levels with respect to unfractionated lymphocytes and purified CD19+ B cells, obtained from 15 normal blood donors. Of note, in a subset of B-CLL samples, the addition to B-CLL cultures of a TRAIL-R1-Fc chimera, which binds at high affinity to surface TRAIL, significantly decreased the percentage of viable cells with respect to untreated control B-CLL cells, suggesting that surface TRAIL may play an unexpected role in promoting B-CLL cell survival. In spite of the majority of B-CLL lymphocytes expressed variable surface levels of "death receptors" TRAIL-R1 and TRAIL-R2, the addition in culture of recombinant TRAIL increased (>20% vs. controls) the degree of spontaneous apoptosis in only 11/44 of the B-CLL samples, had no effect in 19/44, while it significantly increased leukemic cell survival in 14/44. Taken together, these findings suggest that an aberrant expression of TRAIL might contribute to the pathogenesis of B-CLL by promoting the survival in a subset of B-CLL cells
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