2008/04/08

Loss of GNMT induces liver cancer

A team at CIC bioGUNE, in collaboration with investigators at the University of Vanderbilt, the CNIO, and the Keck School of Medicine, have discovered that knockout mice deficient in GNMT, the main enzyme responsible for catabolism of excess hepatic S-adenosylmethionine (SAMe), spontaneously develop fatty liver disease, fibrosis and hepatocellular carcinoma (HCC). Loss of GNMT results in aberrant methylation of DNA and histones resulting in epigenetic modulation of critical carcinogenesis pathways. These findings are of clinical interest, since GNMT is down-regulated in patients at risk of developing HCC, such as in hepatitis C virus- and alcohol-induced liver cirrhosis. These results have been published in HEPATOLOGY.