Key result
Obesity contributes to cancer development through growth factor signaling and chronic inflammation, providing mechanistic targets for disrupting the obesity-cancer link.
Highlights the role of chronic inflammation and growth factor signaling in the obesity-cancer link, providing potential mechanistic targets for intervention.
No practice change from mechanistic review alone; leaves open clinical translation of these pathway targets.
The prevalence of obesity, an established risk factor for many cancers, has risen steadily for the past several decades in the United States and in many parts of the world. This review synthesizes the evidence on key biological mechanisms underlying the obesity-cancer link, with particular emphasis on the impact of energy balance modulation, such as diet-induced obesity and calorie restriction, on growth factor signaling pathways and inflammatory processes. Particular attention is placed on the proinflammatory environment associated with the obese state, specifically highlighting the involvement of obesity-associated hormones/growth factors in crosstalk between macrophages, adipocytes, and epithelial cells in many cancers. Understanding the contribution of obesity to growth factor signaling and chronic inflammation provides mechanistic targets for disrupting the obesity-cancer link.
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Harvey et al. (2011) conducted a review in Obesity and cancer. Obesity was evaluated. Obesity contributes to cancer development through growth factor signaling and chronic inflammation, providing mechanistic targets for disrupting the obesity-cancer link.
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