| Literature DB >> 26301494 |
Jean-Charles Nault1,2,3,4,5, Shalini Datta1,2,3,4, Sandrine Imbeaud1,2,3,4, Andrea Franconi1,2,3,4, Maxime Mallet1,2,3,4, Gabrielle Couchy1,2,3,4, Eric Letouzé1,2,3,4, Camilla Pilati1,2,3,4, Benjamin Verret1,4, Jean-Frédéric Blanc6,7,8, Charles Balabaud7,8, Julien Calderaro1,2,3,4,9, Alexis Laurent10,11, Mélanie Letexier12, Paulette Bioulac-Sage7,8,13, Fabien Calvo1,2,3,4,14, Jessica Zucman-Rossi1,2,3,4,15.
Abstract
Hepatocellular carcinomas (HCCs) are liver tumors related to various etiologies, including alcohol intake and infection with hepatitis B (HBV) or C (HCV) virus. Additional risk factors remain to be identified, particularly in patients who develop HCC without cirrhosis. We found clonal integration of adeno-associated virus type 2 (AAV2) in 11 of 193 HCCs. These AAV2 integrations occurred in known cancer driver genes, namely CCNA2 (cyclin A2; four cases), TERT (telomerase reverse transcriptase; one case), CCNE1 (cyclin E1; three cases), TNFSF10 (tumor necrosis factor superfamily member 10; two cases) and KMT2B (lysine-specific methyltransferase 2B; one case), leading to overexpression of the target genes. Tumors with viral integration mainly developed in non-cirrhotic liver (9 of 11 cases) and without known risk factors (6 of 11 cases), suggesting a pathogenic role for AAV2 in these patients. In conclusion, AAV2 is a DNA virus associated with oncogenic insertional mutagenesis in human HCC.Entities:
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Year: 2015 PMID： 26301494 DOI： 10.1038/ng.3389
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330