LIPID METABOLISM DISORDERS In PANCREATIC CANCER

Abstract

In pancreatic cancer (PC) proved the role of obesity not only as a PC risk factor, but also as a factor associated with reduced survival in PC in adulthood. In PC is marked by increased lipogenesis: an increased need of cancer cells in the fatty acid (FA) is implemented not only by increasing lipogenesis de novo, but also by the exogenous FA assimilation, although several meta-analyses have not confirmed the importance of dietary fat in increasing the PC risk. Metabolic reprogramming of cancer cells is aimed at ensuring the rapid proliferation of tumor cells: the transition to aerobic glycolysis, increased expression of enzymes involved in the FA formation (citrate-synthase, ATP-citrate lyase and FA synthase - FASN), due to a mutation of the gene TP53 . As therapeutic agents in PC offer to inhibit FASN, and also impact prenylation and post-prenylation of oncogenes, in particular, KRAS , known as drugs, given the pleiotropic effect of atorvastatin and newly synthesized inhibitor farnesyltransferase R115777.

Keywords

• kras
• lipid metabolism
• pancreatic cancer
• gene tp53
• fatty acids