Obesity, defined as the abnormal or excessive expansion of white adipose tissue, has reached pandemic proportions and is recognized as an important health concern since it is a common root for several comorbidities, including
malignancies. Indeed, the current knowledge of the white adipose tissue, which shifts its role from an energy storage tissue to an important endocrine and metabolic organ, has opened up new avenues for the discovery of
obesity's effects on
tumor biology. In this review, we will report the epidemiological studies concerning the strong impact of
obesity in several types of
cancer and describe the mechanisms underlying the heterotypic signals between
cancer cell lines and adipocytes, with particular emphasis on
inflammation, the
insulin/IGF-1 axis, and
adipokines. Among the
adipokines, we will further describe the in vitro, in vivo, and clinical data concerning the role of
leptin, recognized as one of the most important mediators of
obesity-associated
cancers. In fact,
leptin physiologically regulates energy metabolism, appetite, and reproduction, and several studies have also described the role of
leptin in affecting
cancer development and progression. Finally, we will summarize the newest pharmacological strategies aimed at mitigating the protumorigenic effects of
leptin, underlining their mechanisms of action.