There is a strong relationship between metabolism and immunity, which can become deleterious under conditions of metabolic stress. Obesity, considered a chronic inflammatory disease, is one example of this link. Chronic inflammation is increasingly being recognized as an etiology in several cancers, particularly those of epithelial origin, and therefore a potential link between obesity and cancer. In this review, the connection between the different factors that can lead to the chronic inflammatory state in the obese individual, as well as their effect in tumorigenesis, is addressed. Furthermore, the association between obesity, inflammation, and esophageal, liver, colon, postmenopausal breast, and endometrial cancers is discussed. 1. Introduction Cancer development is complex and involves different phases commonly referred to as initiation, promotion, and progression [1]. It is believed that during the initiation phase, genetic mutations accumulate that lead to irreversible cellular changes. Some of the most significant changes during this phase include activation of protooncogenes (e.g., ras, bcl2, myc, abl) and inactivation of tumor suppressor genes (e.g., p53, Rb) [1]. These genome-level events give a selective growth or survival advantage to the cell, which confer on cancer cells their intrinsic properties, including self-sufficient proliferation, insensitivity to antiproliferative signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, invasion, and metastasis [2]. Tumor development is promoted by the clonal expansion of these changed cells, and it is followed by the progression phase, which involves tumor growth and metastasis [3]. Determining what causes a particular cancer is a complex task. Many things are known to increase the risk of cancer, including environmental pollutants [4–6], certain infections [7, 8], certain metabolic disorders [9, 10], and so forth. For example, skin cancer has been linked to radiation therapy; viral infections such as the human papilloma virus; exposure to UV radiation; aging; skin color; diet; smoking (reviewed in [11]). Cancer cell initiation, promotion, and progression are also intimately linked to their microenvironment. The environment of the cells can directly affect their genetic make-up or, combined with genetic predisposition, help in the cancer development. The tumor infiltrate, composed of angiogenic vascular cells, lymphatic endothelial cells, cancer-associated fibroblastic cells, and immune cells, have been shown to contribute actively to tumorigenesis [12]. The
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