Epigenetic landscape influences the liver cancer genome architecture

Natsuko Hama, Yasushi Totoki, Fumihito Miura, Kenji Tatsuno, Mihoko Saito-Adachi, Hiromi Nakamura, Yasuhito Arai, Fumie Hosoda, Tomoko Urushidate, Shoko Ohashi, Wakako Mukai, Nobuyoshi Hiraoka, Hiroyuki Aburatani, Takashi Ito and Tatsuhiro Shibata ()
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Natsuko Hama: Chuo-ku
Yasushi Totoki: Chuo-ku
Fumihito Miura: Kyushu University Graduate School of Medical Sciences, Higashi-ku
Kenji Tatsuno: The University of Tokyo
Mihoko Saito-Adachi: Chuo-ku
Hiromi Nakamura: Chuo-ku
Yasuhito Arai: Chuo-ku
Fumie Hosoda: Chuo-ku
Tomoko Urushidate: The University of Tokyo, Minato-ku
Shoko Ohashi: Chuo-ku
Wakako Mukai: Chuo-ku
Nobuyoshi Hiraoka: National Cancer Center Hospital, Chuo-ku
Hiroyuki Aburatani: The University of Tokyo
Takashi Ito: Kyushu University Graduate School of Medical Sciences, Higashi-ku
Tatsuhiro Shibata: Chuo-ku

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract The accumulations of different types of genetic alterations such as nucleotide substitutions, structural rearrangements and viral genome integrations and epigenetic alterations contribute to carcinogenesis. Here, we report correlation between the occurrence of epigenetic features and genetic aberrations by whole-genome bisulfite, whole-genome shotgun, long-read, and virus capture sequencing of 373 liver cancers. Somatic substitutions and rearrangement breakpoints are enriched in tumor-specific hypo-methylated regions with inactive chromatin marks and actively transcribed highly methylated regions in the cancer genome. Individual mutation signatures depend on chromatin status, especially, signatures with a higher transcriptional strand bias occur within active chromatic areas. Hepatitis B virus (HBV) integration sites are frequently detected within inactive chromatin regions in cancer cells, as a consequence of negative selection for integrations in active chromatin regions. Ultra-high structural instability and preserved unmethylation of integrated HBV genomes are observed. We conclude that both precancerous and somatic epigenetic features contribute to the cancer genome architecture.

Date: 2018
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DOI: 10.1038/s41467-018-03999-y

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