Mechanisms of obesity-induced gastrointestinal neoplasia

Abstract

Obesity is among the fastest growing diseases worldwide; treatment is inadequate, and associated disorders, including gastrointestinal cancers, have high morbidity and mortality. An increased understanding of the mechanisms of obesity-induced carcinogenesis is required to develop methods to prevent or treat these cancers. In this report, we review the mechanisms of obesity-associated colorectal, esophageal, gastric, and pancreatic cancers and potential treatment strategies.

Keywords: BE; BMI; Barrett's esophagus; CRC; Colorectal Cancer; EAC; Esophageal Cancer; GCA; GI; Gastric Cancer; IGF; IGFBP; IGFR; IL; IR; LPS; MAPK; MCP-1; MSI; PAC; Pancreatic Cancer; RR; TNF; body mass index; colorectal cancer; esophageal adenocarcinoma; gastric adenocarcinoma; gastrointestinal; insulin receptor; insulin-like growth factor; insulin-like growth factor binding protein; insulin-like growth factor receptor; interleukin; lipopolysaccharides; mTOR; mammalian target of rapamycin; microsatellite instability; mitogen-activated protein kinase; monocyte chemoattractant protein 1; pancreatic adenocarcinoma; relative risk; sTNFR2; soluble tumor necrosis factor receptor 2; tumor necrosis factor.