Abstract
Abstract Liver cancer is prevalent worldwide, mainly associated with virus infection and chronic inflammation, but its underlying molecular mechanism is quite heterogeneous. We performed virome and immuno-genomic analyses, in addition to whole-genome landscape of somatic alterations and transcriptome in 300 liver cancers. Our whole-genome analysis elucidated point mutations in non-coding regions, structural variations, and virus integrations (HBV and AAV), in addition to coding mutations. We discovered novel recurrently mutated coding and non-coding regions, such as NEAT1/MALAT1 lincRNAs, promoters, CTCF-binding sites, and novel regulatory regions, and known cancer genes (CDKN2A, APC, TERT) and novel cancer genes (ASH1L, NCOR1, MACROD2) that were recurrently affected by SVs. For virome analysis, we performed ultra-deep sequencing after capturing HBV sequences from DNAs of 100 liver cancers or adjacent HBV-infected liver tissues, which demonstrated genome-wide HBV-integrations (1794 sites) in liver cancers and infected liver tissues and eliminated pathological mechanism of viral integration. We also generated immuno-genomic profiles of these liver cancers, including HLA genotypes and mutations, neo-antigen presentation, immune signatures, and TCR repertories, which suggested some distinct immunological features and underlying molecular pathways of liver cancer associated with inflammation. These trans-omics data demonstrated comprehensive and distinct immuno-genomic feature of virus-related liver cancer, as well as its distinct whole-genome profiles, and can help to understand the molecular and microenvironment pathways underlying carcinogenesis and treatment response of liver cancer. Citation Format: Hidewaki Nakagawa. Whole-genome, virome, and immuno-genome of liver cancer indicate its genomic feature associated with virus infection and inflammation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4394. doi:10.1158/1538-7445.AM2017-4394
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