Receptor of advanced glycation end-products axis and gallbladder cancer: A forgotten connection that we should reconsider

Abstract

Compelling evidence derived from clinical and experimental research has demonstrated the crucial contribution of chronic inflammation in the development of neoplasms, including gallbladder cancer. In this regard, data derived from clinical and experimental studies have demonstrated that the receptor of advanced glycation end-products (RAGE)/AGEs axis plays an important role in the onset of a crucial and long-lasting inflammatory milieu, thus supporting tumor growth and development. AGEs are formed in biological systems or foods, and food-derived AGEs, also known as dietary AGEs are known to contribute to the systemic pool of AGEs. Once they bind to RAGE, the activation of multiple and crucial signaling pathways are triggered, thus favoring the secretion of several proinflammatory cytokines also involved in the promotion of gallbladder cancer invasion and migration. In the present review, we aimed to highlight the relevance of the association between high dietary AGEs intakes and high risk for gallbladder cancer, and emerging data supporting that dietary intervention to reduce gallbladder cancer risk is a very attractive approach that deserves much more research efforts.

Chronic hyperglycemia and intracranial meningiomas

“…Furthermore, the presence and accumulation of AGEs in different cell types are known to significantly alter both the intracellular as well as the extracellular structure and function, primarily influencing specific genes and transcription factors, and ultimately leading to diabetes and cancer [ 47 ]. Indeed, the presence of AGEs is known to correlate significantly with the development of various neoplasms such as gallbladder [ 48 ], hepatocellular, prostate and breast cancer [ 49 ]. Similar findings have been confirmed in meningiomas as well, where glycation was shown to cause changes in the expression of enzymes with a known role in tumor progression [ 50 ] as well as an increase in the invasion of a meningioma [ 51 ].…”