La Leucémie Myéloïde Chronique Pédiatrique: Une Entité Très Rare Au Service d’Hématologie De Yopougon

Contexte: La leucémie myéloïde chronique (LMC) est un syndrome myéloprolifératif dû à une prolifération myéloïde monoclonale prédominant sur la lignée granuleuse. Son pronostic a été amélioré par l’avènement des inhibiteurs de la tyrosine kinase. Elle survient le plus souvent chez l’adulte jeune. Les auteurs rapportent un cas clinique chez un enfant de 6 ans. Présentation de cas: Il s’agissait d’un enfant de 6 ans, de sexe masculin, référé en consultation en hématologie pour splénomégalie volumineuse évoluant depuis 3 mois. L’hémogramme a montré une hyperleucocytose à 282 Giga/L avec myélémie importante et polymorphe une anémie à 66 g/l et une thrombocytose à 870G/L. L’examen cytogénétique a retrouvé le chromosome Philadelphie sans anomalie additionnelle. Le traitement par imatinib mesylate a pu être débuté. Conclusion: La leucémie myéloïde chronique est certes rare chez l’enfant mais les praticiens doivent y penser devant une hyperleucytose importante persistente. Background: Chronic myeloid leukemia (CML) is a myeloproliferative syndrome due to monoclonal myeloid proliferation predominant over the granular line. His prognosis was improved by the advent of tyrosine kinase inhibitors. It occurs most often in young adults. The authors report the clinical case of a 6-year-old child because of its rarity. Case report: This was a 6-year-old male child, referred in hematology consultation for persistent of large splenomegaly. The hemogram showed hyperleucocytosis at 282 Giga/L with large myelemia and polymorphic anemia at 66 g/l and thrombocytosis at 870 G/L. the cytogenetic analyse found the Philadelphia chromosome without additional anomaly. The treatment with imatinib mesylate has therefore begun. Conclusion: Although the CML is uncommon at young people, but practicians must think about it when we have an important hyperleucocytosis

In silico identification and characterization of putative differentially expressed genes involved in common bean (Phaseolus vulgaris L.) seed development

peer reviewe

A worldwide map of Plasmodium falciparum K13-propeller polymorphisms

Recent gains in reducing the global burden of malaria are threatened by the emergence of Plasmodium falciparum resistance to artemisinins. The discovery that mutations in portions of a P. falciparum gene encoding kelch (K13)-propeller domains are the major determinant of resistance has provided opportunities for monitoring such resistance on a global scale.; We analyzed the K13-propeller sequence polymorphism in 14,037 samples collected in 59 countries in which malaria is endemic. Most of the samples (84.5%) were obtained from patients who were treated at sentinel sites used for nationwide surveillance of antimalarial resistance. We evaluated the emergence and dissemination of mutations by haplotyping neighboring loci.; We identified 108 nonsynonymous K13 mutations, which showed marked geographic disparity in their frequency and distribution. In Asia, 36.5% of the K13 mutations were distributed within two areas--one in Cambodia, Vietnam, and Laos and the other in western Thailand, Myanmar, and China--with no overlap. In Africa, we observed a broad array of rare nonsynonymous mutations that were not associated with delayed parasite clearance. The gene-edited Dd2 transgenic line with the A578S mutation, which expresses the most frequently observed African allele, was found to be susceptible to artemisinin in vitro on a ring-stage survival assay.; No evidence of artemisinin resistance was found outside Southeast Asia and China, where resistance-associated K13 mutations were confined. The common African A578S allele was not associated with clinical or in vitro resistance to artemisinin, and many African mutations appear to be neutral. (Funded by Institut Pasteur Paris and others.)