Federica Biello1, Francesca Platini2, Francesca D'Avanzo2, Carlo Cattrini2, Alessia Mennitto2, Silvia Genestroni2, Veronica Martini2,3, Paolo Marzullo1,4, Gianluca Aimaretti1, Alessandra Gennari1. 1. Department of Translational Medicine, University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy. 2. Division of Oncology, University Hospital "Maggiore della Carità", 28100 Novara, Italy. 3. Lab of Immuno-Oncology, CAAD, Center of Autoimmune and Allergic Disease, University of Eastern Piedmont, 28100 Novara, Italy. 4. Division of General Medicine, IRCCS Istituto Auxologico Italiano, Ospedale S. Giuseppe, 28921 Piancavallo-Verbania, Italy.
Abstract
BACKGROUND: Breast cancer (BC) is the most common neoplasm in women. Many clinical and preclinical studies investigated the possible relationship between host metabolism and BC. Significant differences among BC subtypes have been reported for glucose metabolism. Insulin can promote tumorigenesis through a direct effect on epithelial tissues or indirectly by affecting the levels of other modulators, such as the insulin-like growth factor (IGF) family of receptors, sex hormones, and adipokines. The potential anti-cancer activity of metformin is based on two principal effects: first, its capacity for lowering circulating insulin levels with indirect endocrine effects that may impact on tumor cell proliferation; second, its direct influence on many pro-cancer signaling pathways that are key drivers of BC aggressiveness. METHODS: In the present review, the interaction between BC, host metabolism, and patients' prognosis has been reviewed across available literature evidence. CONCLUSIONS: Obesity, metabolic syndrome, and insulin resistance are all involved in BC growth and could have a relevant impact on prognosis. All these factors act through a pro-inflammatory state, mediated by cytokines originated in fat tissue, and seem to be related to a higher risk of BC development and worse prognosis.
BACKGROUND:Breast cancer (BC) is the most common neoplasm in women. Many clinical and preclinical studies investigated the possible relationship between host metabolism and BC. Significant differences among BC subtypes have been reported for glucose metabolism. Insulin can promote tumorigenesis through a direct effect on epithelial tissues or indirectly by affecting the levels of other modulators, such as the insulin-like growth factor (IGF) family of receptors, sex hormones, and adipokines. The potential anti-cancer activity of metformin is based on two principal effects: first, its capacity for lowering circulating insulin levels with indirect endocrine effects that may impact on tumor cell proliferation; second, its direct influence on many pro-cancer signaling pathways that are key drivers of BC aggressiveness. METHODS: In the present review, the interaction between BC, host metabolism, and patients' prognosis has been reviewed across available literature evidence. CONCLUSIONS:Obesity, metabolic syndrome, and insulin resistance are all involved in BC growth and could have a relevant impact on prognosis. All these factors act through a pro-inflammatory state, mediated by cytokines originated in fat tissue, and seem to be related to a higher risk of BC development and worse prognosis.
Entities:
Keywords:
BMI; IGF; breast cancer; host metabolism; insulin resistance
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