https://www.selleckchem.com/products/s-propranolol-hydrochloride.html 29). BMI was directly correlated with gland volume (P < 0.01). An increase of 1.0 kg/m2 in BMI predicted an increase in parotid volume by 1.1 mL. Male sex was also associated with significantly greater parotid volume. Mean parotid volume increased over time but these gains were driven by increases in BMI and not age alone. These findings are highly relevant to the treatment of the aging face and neck. Mean parotid volume increased over time but these gains were driven by increases in BMI and not age alone. These findings are highly relevant to the treatment of the aging face and neck.In the past two decades, a ponderous epidemiological literature has causally linked tumor onset to environmental exposure to carcinogens. As consequence, risk assessment studies have been carried out with the aim to identify both predictive models of estimating cancer risks within exposed populations and establishing rules for minimizing hazard when handling carcinogenic compounds. The central assumption of these works is that neoplastic transformation is directly related to the mutational burden of the cell without providing further mechanistic clues to explain increased cancer onset after carcinogen exposure. Nevertheless, in the last few years, a growing number of studies have implemented the traditional models of cancer etiology, proposing that neoplastic transformation is a complex process in which several parameters and crosstalk between tumor and microenvironmental cells must be taken into account and integrated with mutagenesis. In this conceptual framework, the current strategies of risk assessment that are solely based on the 'mutator model' require an urgent update and revision to keep pace with advances in our understanding of cancer biology. We will approach this topic revising the most recent theories on the biological mechanisms involved in tumor formation in order to envision a roadmap leading to a fut