Publications by authors named "Arthur Moellman-Coelho"

Despite the favorable clinical evolution of patients with chronic myeloid leukemia (CML), resistance or intolerance to imatinib is present in approximately 35% of patients. Sokal score is a widely used risk factor, however efflux and influx transporters are provisional risk factors implicated in imatinib resistance. This study analyzed Sokal score, ABCB1, ABCG2 and OCT1 mRNA transporter expression levels as well as P-glycoprotein expression and efflux transporters activity to seek a possible correlation between these factors and the molecular response at 12 months from imatinib start as well as 8-year overall survival (OS).

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Resistance to tyrosine-kinase inhibitors is a serious problem in the treatment of chronic myeloid leukemia (CML). Using Western blot, real-time qRT-PCR and flow cytometry, we investigated the expression of survivin, Smac/DIABLO and P-glycoprotein (Pgp) in patients with CML. Survivin overexpression has been associated with cancer progression, multidrug resistance, poor prognosis and short survival in several types of neoplasms including hematological malignancies.

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Despite the relevant therapeutic progresses obtained with imatinib, clinical resistance to this drug has emerged and reemerged after cytogenetic remission in a group of patients with chronic myeloid leukemia (CML). Therefore, novel treatment strategies are needed. In this study, we evaluated the anti-CML activity and mechanisms of action of LQB-118, a pterocarpanquinone structurally related to lapachol [2-hydroxy-3-(3-methyl-2-butenyl)-1,4-naphthoquinone].

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Purpose: To treat non-Hodgkin's B-cell lymphoma (B-NHL) in children with manageable toxicity-related morbidity and without any decrease in survival.

Patients And Methods: Between January 1998 and April 2003, 53 consecutive patients (age 16 years or less) from a single institution were enrolled. The patients were stratified by risk factors (stage and LDH level) and treated with a BFM 86/90 (Berlin-Frankfurt-Münster)-based protocol with reduction of the methotrexate dose from 5 mg/m to 2 mg/m.

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Objectives: The TP53 gene encodes a nuclear protein implicated in the regulation of the cell cycle, DNA repair, and apoptosis. TP53 mutations and other alterations have been described in numerous types of tumors, and some of these have been associated with poor prognosis. The aim of this study was to characterize TP53 mutations in childhood B non-Hodgkin's lymphoma, their correlation with clinical prognostic factors and response to therapy.

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