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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

DOI

10.1158/2159-8290.cd-19-0696

Type

Journal article

Journal

Cancer discovery

Publication Date

08/2019

Volume

9

Pages

1003 - 1005

Addresses

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

Keywords

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