Bugs and food: a recipe for cancer?

Abstract

Obesity and the associated state of subchronic inflammation are risk factors for numerous pathologies, including carcinogenesis. Recently, Schulz et al. (2014) demonstrated that high-fat diet-induced intestinal dysbiosis promotes cancer development in K-ras(G12Dint) mice without inducing obesity or mucosal inflammation, positioning microbial activities as a central component of diet-induced carcinogenesis.

Figure 1. High-Fat Diet-Induced Dysbiosis Promotes Cancer Development in K-ras^G12Dint Mice

Decreased cryptdin expression caused by K-ras oncogene activation, coupled with decreased Muc2 expression from high-fat diet consumption, leads to a distinct shift in the microbiota. This dysbiosis is characterized by decreased butyrate production and leads to increased cancer occurrence. MyD88 signaling is implicated in the disease progression, perhaps by both promoting a proliferative signal and influencing the population of butyrate-producing bacteria, as this short-chain fatty acid prevents proliferation of tumor-initiated epithelial cells.