Leukemia & lymphoma
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Leukemia & lymphoma · Jul 2011
ReviewMyeloproliferative neoplasms 5 years after discovery of JAK2V617F: what is the impact of JAK2 inhibitor therapy?
The watershed discovery of the JAK2V617F mutation in 2005, and the high prevalence of this mutation in the Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs), has led to a renaissance in the science and therapy of these disorders. Inhibitors of JAK2 entered clinical trials in 2007 and ushered in an unprecedented era of trials with agents specifically designed for MPNs. Currently 10 different JAK2 inhibitors have been tested in myelofibrosis (MF) with varying degrees of specificity for the JAK2 kinase. ⋯ However, the ability of these agents to significantly impact disease-associated cytopenias, JAK2 allele burden, or bone marrow histologic features remains unclear. JAK2 inhibition in polycythemia vera (PV) and essential thrombocythemia (ET) for this class of agents appears promising to reduce myeloproliferations, symptoms, and perhaps prevent thrombohemorrhagic events. Alternative agents (with alternative targets), used either alone or in combination, might perhaps further augment the spectrum of efficacy and therapeutic options for MPNs.
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Leukemia & lymphoma · Jun 2011
Multicenter Study Clinical TrialDose-dense high-dose methylprednisolone and rituximab in the treatment of relapsed or refractory high-risk chronic lymphocytic leukemia.
This study evaluated the efficacy and safety of dose-dense high-dose methylprednisolone (HDMP) plus rituximab (Rtx) in patients with high-risk CLL. Twenty-nine patients with relapsed or progressive CLL with adverse cytogenetics (17p deletion, TP53 mutation, 11q deletion, and/or trisomy 12) and/or progression within 12 months of fludarabine treatment were included. HDMP (1 g/m(2)) was administered daily for 5 days of each treatment course. ⋯ After 22 months, the median progression-free and overall survivals were 12 and 31 months, respectively. The most frequent toxicity was hyperglycemia, and three deaths occurred in the study. Dose-dense treatment with HDMP and Rtx is an effective therapy with a favorable safety profile in patients with high-risk CLL, including those with 17p deletion/TP53 mutation.