Laboratory of Cellular Biology

Rio de Janeiro, Brazil

Laboratory of Cellular Biology

Rio de Janeiro, Brazil
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Micol J.B.,University Paris Diderot | Raffoux E.,University Paris Diderot | Boissel N.,University Paris Diderot | Lengline E.,University Paris Diderot | And 10 more authors.
European Journal of Cancer | Year: 2014

Purpose Acute promyelocytic leukaemia (APL) therapy with all-trans retinoic acid and chemotherapy is associated with a high cure rate in clinical trials. As some patients are not enrolled in these trials due to early severe events, these results might be overestimated. To address this issue, we reviewed all APL patients referred to the Hospital Saint-Louis within the 2000-2010 period, with a special focus on inclusion in recruiting trials. Patients and methods One hundred patients (including eight children) with newly diagnosed APL were admitted during this period, which covered two consecutive APL trials conducted by the French-Belgian-Swiss APL group. Results The rate of patients not enrolled within recruiting trials was 29%. The main reason for non-inclusion was protocol ineligibility related to disease severity at diagnosis. Non-enrolled patients more frequently had white blood cell count (WBC) ≥ 50 × 109/L (31% versus 8%; p =.01), platelet count < 40 × 10 9/L (97% versus 65%; p =.001) and microgranular variant APL (38% versus 11%; p =.004) and were more frequently admitted in intensive care unit during induction (41% versus 24%; p =.094). Early mortality rate was higher in non-enrolled patients (21% versus 3%; p =.007), translating into a lower complete remission rate (79% versus 96%; p =.007) and lower event-free survival (65% versus 84% at 5 years; p =.05), while disease-free survival was similar in both non-enrolled and enrolled patient groups (81% versus 88% at 5 years; p =.68). Conclusion Initial APL severity leads to a significant proportion of patients non-registered within clinical trials, which may underestimate the real early mortality, which remained nonetheless less than 10% in this study. © 2014 Elsevier Ltd. All rights reserved.


Jardim G.A.M.,Federal University of Minas Gerais | Reis W.J.,Federal University of Minas Gerais | Ribeiro M.F.,Federal University of Minas Gerais | Ottoni F.M.,Federal University of Minas Gerais | And 8 more authors.
RSC Advances | Year: 2015

In our continued search for novel trypanocidal compounds, arylamine, chalcone, triazolic, triazole-carbohydrate and chalcogenium derivatives containing a naphthoquinone scaffold were prepared; in addition to electrochemical studies, these compounds were evaluated against the infective bloodstream form of Trypanosoma cruzi, the etiological agent of Chagas disease. Among the thirty-eight compounds herein evaluated, six were found to be more potent against trypomastigotes than the standard drug benznidazole, with IC50/24 h values between 52.9 and 89.5 μM. © The Royal Society of Chemistry 2015.


PubMed | Laboratory of Cellular Biology
Type: Journal Article | Journal: Autophagy | Year: 2010

Lafora disease (LD) is a progressive, lethal, autosomal recessive, neurodegenerative disorder that manifests with myoclonus epilepsy. LD is characterized by the presence of intracellular inclusion bodies called Lafora bodies (LB), in brain, spinal cord and other tissues. More than 50 percent of LD is caused by mutations in EPM2A that encodes laforin. Here we review our recent findings that revealed that laforin regulates autophagy. We consider how autophagy compromise may predispose to LB formation and neurodegeneration in LD, and discuss future investigations suggested by our data.

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