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Mutational landscape of intrahepatic cholangiocarcinoma

Author

Listed:
  • Shanshan Zou

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

  • Jiarui Li

    (Simon Fraser University
    Fudan University)

  • Huabang Zhou

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

  • Christian Frech

    (Simon Fraser University)

  • Xiaolan Jiang

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

  • Jeffrey S. C. Chu

    (Wuhan Frasergen Bioinformatics Co. Ltd)

  • Xinyin Zhao

    (Simon Fraser University)

  • Yuqiong Li

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

  • Qiaomei Li

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

  • Hui Wang

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

  • Jingyi Hu

    (School of Medicine, Jiao Tong University
    Present address: Department of Digestive Diseases, Huashan Hospital, Fudan University, 12 Middle Wulumuqi Road, Shanghai 200040, China)

  • Guanyi Kong

    (Wuhan Frasergen Bioinformatics Co. Ltd)

  • Mengchao Wu

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

  • Chuanfan Ding

    (Fudan University)

  • Nansheng Chen

    (Simon Fraser University)

  • Heping Hu

    (Eastern Hepatobiliary Surgery Hospital, Second Military Medical University)

Abstract

Intrahepatic cholangiocarcinoma (ICC) is a fatal primary liver cancer (PLC) that affects 5–10% of all PLCs. Here we sequence tumour and matching control sample pairs of a large cohort of 103 ICC patients in China, resulting in the identification of an ICC-specific somatic mutational signature that is associated with liver inflammation, fibrosis and cirrhosis. We further uncover 25 significantly mutated genes including eight potential driver genes (TP53, KRAS, IDH1, PTEN, ARID1A, EPPK1, ECE2 and FYN). We find that TP53-defective ICC patients are more likely to be HBsAg-seropositive, whereas mutations in the oncogene KRAS are nearly exclusively found in HBsAg-seronegative ICC patients. Three pathways (Ras/phosphatidylinositol-4,5-bisphosphate 3-kinase signalling, p53/cell cycle signalling and transforming growth factor-β/Smad signalling), genes important for epigenetic regulation and oxidative phosphorylation are substantially affected in ICC. We reveal mutations in this study that may be valuable for designing further studies, better diagnosis and effective therapies.

Suggested Citation

  • Shanshan Zou & Jiarui Li & Huabang Zhou & Christian Frech & Xiaolan Jiang & Jeffrey S. C. Chu & Xinyin Zhao & Yuqiong Li & Qiaomei Li & Hui Wang & Jingyi Hu & Guanyi Kong & Mengchao Wu & Chuanfan Ding, 2014. "Mutational landscape of intrahepatic cholangiocarcinoma," Nature Communications, Nature, vol. 5(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6696
    DOI: 10.1038/ncomms6696
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    Cited by:

    1. Yaodong Zhang & Zijian Ma & Changxian Li & Cheng Wang & Wangjie Jiang & Jiang Chang & Sheng Han & Zefa Lu & Zicheng Shao & Yirui Wang & Hongwei Wang & Chenyu Jiao & Dong Wang & Xiaofeng Wu & Hongbing , 2022. "The genomic landscape of cholangiocarcinoma reveals the disruption of post-transcriptional modifiers," Nature Communications, Nature, vol. 13(1), pages 1-13, December.

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