Annals of hematology
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Annals of hematology · Mar 2007
Whole blood laboratory model of thrombocytopenia for use in evaluation of hemostatic interventions.
This study describes a laboratory model of whole blood (WB) thrombocytopenia established with blood from healthy volunteers. We obtained a mean platelet count of 16 x 10(9)/l (95% confidence interval, 10-22) in WB by repeatedly replacing the platelet-rich supernatant with autologous platelet-poor plasma from the same individual. ⋯ Control experiments revealed minimal changes in coagulation factors, distribution of bloods cells, and platelet activation capabilities. The WB model appears useful in research, development, and evaluation of the effects of hemostatic interventions in thrombocytopenia.
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Annals of hematology · Dec 2006
Controlled Clinical TrialNot all imatinib resistance in CML are BCR-ABL kinase domain mutations.
Point mutations within the ABL kinase domain of the BCR-ABL gene are associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML). To obtain more information about the association between BCR-ABL mutations and type of imatinib resistance, we studied 30 early chronic phase (CP) CML patients, commencing imatinib therapy, using a conventional sequencing technique. Seven patients treated in late CP and three patients treated in the accelerated phase were included for comparison. ⋯ We conclude that screening early CP patients for BCR-ABL mutations before start of imatinib therapy is not cost-effective. BCR-ABL kinase domain mutations do not appear to explain cytogenetic or molecular (detectable BCR-ABL transcripts by polymerase chain reaction) disease persistence in patients otherwise in stable disease. However, in patients with signs of expanding disease burden, a search for BCR-ABL mutations is warranted.
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Annals of hematology · Nov 2006
Controlled Clinical TrialEffect of rituximab on the long-term outcome after high-dose therapy for relapsed B-cell non-Hodgkin's lymphoma.
To better define the role of rituximab in salvage and high-dose therapy (HDT) for relapsed or refractory non-Hodgkin's lymphoma (NHL), patients treated before the implementation of rituximab in salvage and HDT (n = 57, control group) were compared with patients with rituximab included in this procedure (n = 36, study group). All patients had been antibody-naive at this point, and analyses were performed separately for 22 and 31 patients with aggressive, and 14 and 26 patients with indolent NHL, respectively. All patients received two courses of salvage therapy, predominantly dexamethasone, BCNU, etoposide, cytosine arabinoside, melphalan. ⋯ For patients with indolent lymphoma, no comparable benefit was detectable. Our data support the use of rituximab in HDT for patients with aggressive NHL. For patients with indolent NHL, only longer follow-up and/or randomized trials may help to fully determine the impact of rituximab on the outcome after HDT.