1,720,983 research outputs found
Nilotinib can override dasatinib resistance in chronic myeloid leukemia patients with secondary resistance to imatinib first-line therapy
[No abstract available
Occurrence of colon adenocarcinoma in chronic myeloid leukemia patients treated with imatinib: Report of two cases and review of the literature
[No abstract available
Efficacy of dasatinib in a chronic myeloid leukemia patient with disease molecular relapse and chronic GVHD after haploidentical BMT: AN IMMUNOMODULATORY EFFECT?
Dasatinib, a novel protein tyrosine kinase inhibitor targeting Src family kinases (for example, Lyn, Fyn, Hck) and Abl family kinases, was recently approved for treatment of adult patients with CML, resistant or intolerant to imatinib.1 It potently inhibits the constitutively active BCR–ABL kinase, but also Lck at low picomolar concentrations.2 Recently it was reported that dasatinib specifically targets the earliest events in TCR signaling and enhances the inhibitory effects of CYA, and was thus proposed as a new therapeutic opportunity to address autoimmune diseases, GVHD and transplant allograft rejection.
Cardiac events in imatinib mesylate-treated chronic myeloid leukemia patients: A single institution experience
[No abstract available
Achievement of complete molecular responses in late chronic phase chronic myeloid leukaemia patients treated with pulsed imatinib while in minimal residual disease
Chronic myeloid leukaemia (CML) patients in chronic phase (CP) are currently treated with a standard dose of imatinib of 400 mg/daily. However, once in complete cytogenetic remission (CCR) it is possible that some patients maintain this status with reduced dose of the drug. Here, we describe five cases of CML in late CP, which were switched to imatinib while in CCR after interferon alpha (IFN alpha) and reached complete and stable molecular remission with intermittent drug administration at 400 mg/every 20 days/month. (C) 2008 Elsevier Ltd. All rights reserved
Platelet count is an independent prognostic factor in myelodysplastic syndromes considered as low risk by French-American-British and World Health Organisation classifications.
Fasting glucose improvement under dasatinib treatment in an accelerated phase chronic myeloid leukemia patient unresponsive to imatinib and nilotinib
[No abstract available
Chronic myelomonocytic leukemia with antecedent refractory anemia with excess blasts: Further evidence for the arbitrary nature of current classification systems
From a retrospective analysis of our series of myelodysplastic patients, we found 16 patients who were initially diagnosed as having a refractory anemia with excess of blasts (RAEB) according to FAB criteria, but later on (median time 4 months, range 2-8) developed a peripheral monocytosis >1 x 10(9)/L, leading to a disease re-classification into a dysplastic type of chronic myelomonocytic leukemia (MD-CMML). Analysis of clinical and prognostic aspects in this subgroup of patients as compared with those of primarily diagnosed MD-CMML patients, showed some significant differences in Hb level, platelet count, percentage of immature circulating precursor (IPC), bone marrow blastosis and trilineage dysplasia. Median survival for present group of patients was 33 months compared with 20 months for MD-CMML. Different prognostic scores were applied for evaluation of risk distribution and relative impact on survival prediction. We suggest on a possible atypical presentation of CMML and indicate a careful attention to be addressed to myelodysplastic patients who develop peripheral monocytosis, who might have a CMML variant, with more favourable prognosis and prolonged survival. Furthermore, we believe this is a further evidence for the arbitrary nature of current classification systems, which definitely exclude CMML from myelodysplastic syndromes
Unusual association of paroxysmal cold hemoglobinuria as the first sign of disease in myelodysplastic patient
[No abstract available
Dasatinib overcomes imatinib and nilotinib failure in Philadelphia chromosome positive chronic myeloid leukemia with different mechanisms of resistance
[No abstract available
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