Spontaneous development of hepatocellular carcinoma and B-cell lymphoma in mosaic and heterozygous Brca2 and Cdkn1a interacting protein (Bccip) knockout mice.

In this study, we established a new genetically engineered mouse model with Bccip deficiency. Mosaic or heterozygous Bccip deletion conferred an increased risk of spontaneous liver tumorigenesis and B-cell lymphoma development at old age. These abnormalities are accompanied with chronic inflammation, histology of nonalcoholic steatohepatitis, keratin and ubiquitin aggregates within cytoplasmic Mallory-Denk bodies, and changes of the intra-cellular distribution of high mobility group box 1 protein. Our study suggests BCCIP dysregulation as a risk factor for HCC, and it offers a novel mouse model for future investigations of non-viral or non-alcoholic causes of HCC development. PMID: 32201259 [PubMed - as supplied by publisher]
Source: The American Journal of Pathology - Category: Pathology Authors: Tags: Am J Pathol Source Type: research