20 miliardi di euro l’anno: i costi per il cancro in Italia – Prevenzione attiva, la vera arma vincente
The experimental setup will include the analysis of the bioenergetic parameters (basal, maximal and spare respiratory and glycolytic capacity; respiration and glycolysis devoted to ATP production, proton leak, non-mitochondrial respiration, non-glycolytic acidification, endogenous fatty acid beta-oxidation, ATP index, energy phenotype) of PBMCs and PBMC-derivatives able to detect metabolic dysfunctions relevant to the interception of the colon cancer driver. The Biccocca University research projects are already focused on cancer metabolism profiling, in the perspective of personalised medicine. In these projects, different methodological approaches including Extracellular Flux Analyzer Seahorse, high-content confocal analysis, cytofluorimetry, and multi-omics integration are applied to the study of metabolic rewiring, cellular bioenergetics, nutrient dependency, signal transduction and immunophenotyping in 2D and 3D cellular models, including different solid tumors.
EFFECTS ON SOLUTION
Mitochondrial toxicity, which involves damage or dysfunction of the mitochondria, could potentially serve as a prodromal cancer condition, eg: Mitochondrial DNA Mutations: Mitochondrial DNA due to its proximity to ROS production and its limited DNA repair mechanisms. Apoptosis: Mitochondria play a key role in initiating apoptosis, or programmed cell death. Genetic Changes: could lead to mutations in both mitochondrial DNA (mtDNA) and nuclear DNA; these changes could represent a very early stage of cancer. Metabolic Shift: Mitochondrial toxicity induces a metabolic shift towards glycolysis (Warburg effect), this shift could fuel an uncontrolled cell proliferation that is a hallmark of cancer. Increased Oxidative Stress: can increase the production of reactive oxygen species (ROS), leading to oxidative stress which can contribute to the initiation of cancer. Chronic Inflammation: Mitochondrial toxicity can trigger inflammation.
