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About one third of cases of hepatocellular carcinoma (HCC) show gain-of-function mutations of CTNNB1 (β-catenin) that correlate with sparse intratumoral T-cell content, as observed previously in an ample spectrum of malignancies, and there is mounting preliminary evidence that such HCC cases are refractory to treatment with PD-1 checkpoint inhibitors. Elegant hepatocarcinogenesis experiments by in vivo gene transfer to mouse hepatocytes show that coexpression of active forms of β-catenin result in poor T-cell infiltrates, faster progression in immunocompetent hosts, and unresponsiveness to immunotherapy with checkpoint inhibitors.See related article by Ruiz de Galarreta et al., p. 1124.

Original publication




Journal article


Cancer discovery

Publication Date





1003 - 1005


Program of Immunology and Immunotherapy, Cima Universidad de Navarra, Pamplona, Spain.


Animals, Mice, Carcinoma, Hepatocellular, Liver Neoplasms, beta Catenin, Programmed Cell Death 1 Receptor, Carcinogenesis