Publications by authors named "Manuela Albuquerque de Melo"
The gradual acquisition of genetic and epigenetic disturbances bestows malignant traits upon hematopoietic stem cells, subverting them into a founder and reservoir cell for de novo acute myeloid leukemia (AML) known as leukemic stem cells (LSC). Beyond its molecular heterogeneity, AML is also characterized by rewiring biological processes to support its onset and maintenance. LSC were observed to inherently and actively trigger mitochondrial turnover through selective autophagic removal such that impairing the process led to cell differentiation at the expense of its stemness.
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- Acute myeloid leukemia (AML) is a complex disease with diverse clinical features and significant molecular challenges, particularly related to FLT3 mutations.
- Researchers investigated the interactions between autophagy and the inflammasome to understand how these pathways might impact FLT3 inhibitor effectiveness in treating AML.
- Their findings suggest that autophagy and inflammasome activation are linked to poor responses to FLT3 inhibitors, indicating a need for further study on these pathways to enhance treatment strategies.
Alpha thalassemia, but not β-globin haplotypes, influence sickle cell anemia clinical outcome in a large, single-center Brazilian cohort.
Ann Hematol
April 2021
Alpha thalassemia and beta-globin haplotype are considered classical genetic disease modifiers in sickle cell anemia (SCA) causing clinical heterogeneity. Nevertheless, their functional impact on SCA disease emergence and progression remains elusive. To better understand the role of alpha thalassemia and beta-globin haplotype in SCA, we performed a retrospective study evaluating the clinical manifestations of 614 patients.
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