Abstract

Leading article steatosis itself ‘lubricates’ HCC develop- ment, although we are just beginning to Non-alcoholic fatty liver disease dissect the underlying mechanisms. as a risk factor for hepatocellular MECHANISMS LINKING NAFLD WITH HEPATOCARCINOGENESIS carcinoma: mechanisms and Lipid accumulation in hepatocytes and hepatoma cells induces cancer-related molecular signalling involving nuclear factor implications kappaB (NF-kB) and c-Jun N-terminal kinase(JNK)/activator protein-1 activity, 1 2 and overexpression of tumour growth- Felix Stickel, Claus Hellerbrand 11e14 promoting genes, respectively. For example, unsaturated fatty acids inhibit the The pathophysiological significance of affluent societies, and their significance in expression of phosphatase and tensin hepatic lipid accumulation in the absence the pathophysiology of NAFLD, a rising homologue (PTEN) in hepatocytes via acti- of significant alcohol consumption is incidence of NAFLD and its complica- vation of an NF-kB/mammalian target of 15 16 increasingly recognised. Thus, non-alco- tionsdincluding HCCdcan be expected rapamycin (mTOR) complex. PTEN is holic fatty liver disease (NAFLD) is now in the mid-term future. Therefore, it is a regulator of phosphoinositide 3-kinase considered the most common cause of particularly worrying that the most (PI3K) signalling and an important tumour liver enzyme elevation in Western coun- persuasive evidence for an association suppressor mutated/deleted in HCC, and tries.