« CRISPR-Cas9-engineered mice developing liver cancers with beta-catenin mutation: towards a better understanding of liver carcinogenesis »
One third of hepatocellular carcinoma (HCC) have mutations activating beta-catenin signaling. We definitely showed that these mutations are oncogenic in mice (Loesch et al., J Hepatol 2022), and are responsible for the development of HCC and mesenchymal hepatoblastoma. This mouse model and a previous one obtained through a loss of function of Apc are valuable preclinical models to better understand why a large subset of beta-catenin activated HCCs are resistant to immunotherapies. Our work further supports the hypothesis that they could be treated based on their metabolism (Gougelet et al., Gastroenterol 2019; Senni et al., Gut 2019). Lastly, the CRISPR-Cas9 strategy appears to be an easy-to-use approach to investigate the oncogenic function of specific mutations in HCC.