Aberrant integration of Hepatitis B virus DNA promotes major restructuring of human hepatocellular carcinoma genome architecture
By
Eva G. Alvarez,
Jonas Demeulemeester,
Clemency Jolly,
Daniel Garcia-Souto,
Paula Otero,
Ana Pequeno,
Jorge Zamora,
Marta Tojo,
Javier Temes,
Adrian Baez-Ortega,
Bernardo Rodriguez-Martin,
Yilong Li,
Ana Oitaben,
Alicia L. Bruzos,
Monica Martinez-Fernandez,
Kerstin Haase,
Martin Santamarina,
Sonia Zumalave,
Rosanna Abal,
Jorge Rodriguez-Castro,
Aitor Rodriguez-Casanova,
Angel Diaz-Lagares,
Keiran Raine,
Adam P Butler,
Atsuhi Ono,
Hiroshi Aikata,
Kazuaki Chayama,
Masaki Ueno,
Shinya Hayami,
Hiroki Yamaue,
Miguel G. Blanco,
Xavier Forns,
Carmen Rivas,
Sofia Perez-del-Pulgar,
Raul Torres-Ruiz,
Sandra Rodriguez Perales,
Urtzi Garaigorta,
Hidewaki Nakagawa,
Peter J. Campbell,
Peter Van Loo,
Jose M.C. Tubio
Posted 19 Apr 2021
bioRxiv DOI: 10.1101/2021.04.19.440412
Most cancers are characterized by the somatic acquisition 52 of genomic rearrangements during tumour evolution that eventually drive the oncogenesis. There are different mutational mechanisms causing structural variation, some of which are specific to particular cancer types. Here, using multiplatform sequencing technologies, we identify and characterize a remarkable mutational mechanism in human hepatocellular carcinoma caused by Hepatitis B virus, by which DNA molecules from the virus are inserted into the tumour genome causing dramatic changes in its configuration, including non-homologous chromosomal fusions and megabase-size telomeric deletions. This aberrant mutational process, present in at least 8% of all HCC tumours, is active early during liver cancer evolution and can provide the driver rearrangements that a cancer clone requires to survive and grow.
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