Publications by authors named "Mariana Tannoury"
Article Synopsis
- * The study revealed that CLL cells rely heavily on fatty acid beta-oxidation for energy, and inhibiting the enzyme ACOX1 can shift their metabolism and lead to cell death, even in challenging cases.
- * Combining ACOX1 inhibition with BTK inhibitors showed enhanced effectiveness in eliminating CLL cells while leaving healthy blood cells unharmed, suggesting a promising direction for novel, metabolism-focused therapies.
In addition to intrinsic genomic and nongenomic alterations, tumor progression is also dependent on the tumor microenvironment (TME, mainly composed of the extracellular matrix (ECM), secreted factors, and bystander immune and stromal cells). In chronic lymphocytic leukemia (CLL), B cells have a defect in cell death; contact with the TME in secondary lymphoid organs dramatically increases the B cells' survival via the activation of various molecular pathways, including the B cell receptor and CD40 signaling. Conversely, CLL cells increase the permissiveness of the TME by inducing changes in the ECM, secreted factors, and bystander cells.
View Article and Find Full Text PDFResistance to death is one of the hallmarks of human B cell malignancies and often contributes to the lack of a lasting response to today's commonly used treatments. Drug discovery approaches designed to activate the death machinery have generated a large number of inhibitors of anti-apoptotic proteins from the B-cell lymphoma/leukemia 2 family and the B-cell receptor (BCR) signaling pathway. Orally administered small-molecule inhibitors of Bcl-2 protein and BCR partners (e.
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- - This study focuses on the role of Apoptosis-Inducing Factor (AIF) in mitochondrial function and cell death, highlighting its significance in severe pediatric mitochondrial diseases and cancer progression due to mutations affecting AIF.
- - Researchers created a new AIF-deficient mouse model to investigate the cellular and developmental consequences of AIF loss, using various molecular and cell biology methods to observe changes in cell behavior, metabolism, and overall phenotype.
- - Findings revealed that AIF deficiency disrupts mitochondrial electron transport, leading to ROS overproduction and metabolic reprogramming towards anaerobic glycolysis, with some cells showing resilience by reducing mitochondrial mass and escaping programmed cell death.