At the crossroad between obesity and gastric cancer

Abstract

Obesity has reached epidemic proportions worldwide with disproportionate prevalence in different communities and ethnic groups. Recently, the American Medical Association recognized obesity as a disease, which is a signifi cant milestone that opens the possibilities of treating obesity under standardized health plans. Obesity is an infl ammatory disease characterized by elevated levels of biomarkers associated with abnormal lipid profi les, glucose levels, and blood pressure that lead to the onset of metabolic syndrome. Interestingly, infl ammatory biomarkers, in particular, have been implicated in the risk of developing several types of cancer. Likewise, obesity has been linked to esophageal, breast, gallbladder, kidney, pancreatic, and colorectal cancers. Thus, there exists a link between obesity status and tumor appearance, which may be associated to the differential levels and the circulating profi les of several infl ammatory molecules. For example, mediators of the infl ammatory responses in both obesity and gastric cancer risk are the same: pro- infl ammatory molecules produced by the activated cells infi ltrating the infl amed tissues. These molecules trigger pathways of activation shared by obesity and cancer. Therefore, understanding how these different pathways are modulated would help reduce the impact that both diseases, and their concomitant existence, have on society.