Impact of microbiota-immunity axis in pancreatic cancer management

Abstract

The microbiota impact on human diseases is well-known, and a growing body of literature is providing evidence about the complex interplay between microbiota-immune system-human physiology/pathology, including cancers. Together with the defined risk factors (e.g., smoke habits, diet, diabetes, and obesity), the oral, gut, biliary, and intrapancreatic microbiota contribute to pancreatic cancer development through different pathways including the interaction with the immune system. Unfortunately, a great majority of the pancreatic cancer patients received a diagnosis in advanced stages not amenable to be radically treated and potentially cured. Given the poor pancreatic cancer prognosis, complete knowledge of these complicated relationships could help researchers better understand the disease pathogenesis and thus provide early potential non-invasive biomarkers, new therapeutic targets, and tools for risk stratification that might result in greater therapeutic possibilities and eventually in a better and longer patient survival.

Keywords: Cancer development; Carcinogenesis; Dysbiosis; Gastrointestinal tumors; Gut microbiota; Hepatopancreatobiliary tumors; Pancreatic cancer.

Figure 1

Pathogenetic models. This figure aims at simplifying the complex interplay between microbiota in different anatomical districts and the immune system in carcinogenesis. Each component of the microbiota might be implicated in pancreatic cancer through different pathogenetic mechanisms. LPS: Lipopolysaccharide; NF-kB: Nuclear Factor kB; HBV/HCV: Hepatitis B/C virus; MBL: Mannose-binding lectin; TLR: Toll-like receptor; Treg: T regulatory.