20 miliardi di euro l’anno: i costi per il cancro in Italia – Prevenzione attiva, la vera arma vincente
Potential clients would like to do real cancer prevention through analyses and related interventions that can prevent the development of the disease and not discover it when it is already present, as is the case with early detection. The clients themselves are not motivated to undergo genetic tests that indicate any hereditary conditions (through the analysis of germline mutations) that induce a passive position towards the potential development of the disease because they are not modifiable and are mainly a source of stress.
Potential clients, therefore, would like to prevent cancer with an active attitude through the control and management of physiological and modifiable conditions that promote the development of cancer before the disease is formed. Countless interventions can be made to treat physiological conditions that, if altered, are drivers of tumour development. Still, far fewer interventions can be made once the tumour has already formed.
In addition to the limitations highlighted by traditional prevention, which prevents death from cancer rather than cancer, potential customers are forced to undergo invasive diagnostic techniques like colon cancer.
To fight cancer, it is necessary to know the physiological or pathophysiological conditions from which it originates because intervening when cancer is already formed is a failure. The leading physiological condition that drives cancer development is genomic instability.
In fact, cancer risk factors are associated with the buildup of mutations promoting the transformation of normal cells into cancer cells. Cells that accumulate such mutations are genetically unstable, and genomic instability is a feature of the cancer prodromal phase. Other important cancer drivers (chronic inflammation, immune system imbalance, and altered microbiota), provide an environment favourable to the transition from premalignancy to malignancy. They can both promote or insist on genomic instability, amplifying the cancer risk. Inflammatory cells may produce molecules, such as reactive oxygen species (ROS), that can lead to DNA damage and, consequently, to mutations. An immune cell imbalance can halt the ability of the body’s natural defences to kill cancer cells. The human microbiota (that is, the microbial population living on the organism’s internal and external surfaces) can play a role, too; sometimes, carcinogenesis is linked to the presence of a single bacterial species, whereas in other cases, microbiota imbalance (the so-called dysbiosis) are involved. Bioscience Genomics proposes the HELIXAFE program that enables actionable cancer driver interception and management, starting from monitoring the factors promoting genomic instability, which is the primary driver of cancer development. The first crucial step is analysing the sequence of genes involved in maintaining genomic stability (HELIXBALANCE), such as the ones encoding factors involved in DNA damage response. If mutated, such genes work as cancer driver factors, and their presence should prompt the monitoring of genome instability. The second step included in the program (CYTOBALANCE, IMMUNEBALANCE, MICROBALANCE) allows for the simultaneous monitoring of the secondary drivers of cancer: low-grade chronic inflammation, immune system imbalance, dysbiosis, and mitochondrial toxicity. For each driver condition, BIOSCIENCE GENOMICS developed chemopreventive treatments through which the program ultimately translates the model of CVD active prevention on cancer driver interception, offering the possibility to act before the onset of cancer to counteract the disease well before early diagnosis in healthy individuals, and to monitor the efficiency of the lifestyle and chemoprevention-based strategies put in place to halt its development.
