J Cancer 2016; 7(15):2346-2359. doi:10.7150/jca.16884 This issue
1. Clinical Pathology Laboratory, Department of Experimental Oncology. Giovanni Paolo II National Cancer Institute, V.Le Orazio Flacco 65, 70124 -Bari, Italy.
2. Department of Surgery Oncology. Giovanni Paolo II National Cancer Institute, V.Le Orazio Flacco 65, 70124 -Bari, Italy.
3. Department of Medical Oncology, Giovanni Paolo II National Cancer Institute, V.Le Orazio Flacco 65, 70124 -Bari, Italy.
Adipose tissue in addition to its ability to keep lipids is now recognized as a real organ with both metabolic and endocrine functions. Recent studies demonstrated that in obese animals is established a status of adipocyte hypoxia and in this hypoxic state interaction between adipocytes and stromal vascular cells contribute to tumor development and progression. In several tumors such as breast, colon, liver and prostate, obesity represents a poor predictor of clinical outcomes. Dysfunctional adipose tissue in obesity releases a disturbed profile of adipokines with elevated levels of pro-inflammatory factors and a consequent alteration of key signaling mediators which may be an active local player in establishing the peritumoral environment promoting tumor growth and progression. Therefore, adipose tissue hypoxia might contribute to cancer risk in the obese population. To date the precise mechanisms behind this obesity-cancer link is not yet fully understood. In the light of information provided in this review that aims to identify the key mechanisms underlying the link between obesity and cancer we support that inflammatory state specific of obesity may be important in obesity-cancer link.
Keywords: adipocytes inflammation, adipocytokine, obesity, cancer.