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Aberrant PD-L1 expression through 3′-UTR disruption in multiple cancers

Author

Listed:
  • Keisuke Kataoka

    (Graduate School of Medicine, Kyoto University)

  • Yuichi Shiraishi

    (Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo)

  • Yohei Takeda

    (Graduate School of Medicine, Hokkaido University)

  • Seiji Sakata

    (Pathology Project for Molecular Targets, Cancer Institute, Japanese Foundation for Cancer Research)

  • Misako Matsumoto

    (Graduate School of Medicine, Hokkaido University)

  • Seiji Nagano

    (Institute for Frontier Medical Science, Kyoto University)

  • Takuya Maeda

    (Institute for Frontier Medical Science, Kyoto University)

  • Yasunobu Nagata

    (Graduate School of Medicine, Kyoto University)

  • Akira Kitanaka

    (Faculty of Medicine, University of Miyazaki)

  • Seiya Mizuno

    (Laboratory Animal Resource Center and Faculty of Medicine, University of Tsukuba)

  • Hiroko Tanaka

    (Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo)

  • Kenichi Chiba

    (Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo)

  • Satoshi Ito

    (Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo)

  • Yosaku Watatani

    (Graduate School of Medicine, Kyoto University)

  • Nobuyuki Kakiuchi

    (Graduate School of Medicine, Kyoto University)

  • Hiromichi Suzuki

    (Graduate School of Medicine, Kyoto University)

  • Tetsuichi Yoshizato

    (Graduate School of Medicine, Kyoto University)

  • Kenichi Yoshida

    (Graduate School of Medicine, Kyoto University)

  • Masashi Sanada

    (Clinical Research Center, Nagoya Medical Center)

  • Hidehiro Itonaga

    (Sasebo City General Hospital)

  • Yoshitaka Imaizumi

    (Atomic Bomb Disease and Hibakusya Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University)

  • Yasushi Totoki

    (National Cancer Center Research Institute)

  • Wataru Munakata

    (National Cancer Center Hospital)

  • Hiromi Nakamura

    (National Cancer Center Research Institute)

  • Natsuko Hama

    (National Cancer Center Research Institute)

  • Kotaro Shide

    (Faculty of Medicine, University of Miyazaki)

  • Yoko Kubuki

    (Faculty of Medicine, University of Miyazaki)

  • Tomonori Hidaka

    (Faculty of Medicine, University of Miyazaki)

  • Takuro Kameda

    (Faculty of Medicine, University of Miyazaki)

  • Kyoko Masuda

    (Institute for Frontier Medical Science, Kyoto University)

  • Nagahiro Minato

    (Graduate School of Medicine, Kyoto University)

  • Koichi Kashiwase

    (Japanese Red Cross Kanto-Koshinetsu Block Blood Center)

  • Koji Izutsu

    (Toranomon Hospital)

  • Akifumi Takaori-Kondo

    (Graduate School of Medicine, Kyoto University)

  • Yasushi Miyazaki

    (Atomic Bomb Disease and Hibakusya Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University)

  • Satoru Takahashi

    (Laboratory Animal Resource Center and Faculty of Medicine, University of Tsukuba)

  • Tatsuhiro Shibata

    (National Cancer Center Research Institute
    Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo)

  • Hiroshi Kawamoto

    (Institute for Frontier Medical Science, Kyoto University)

  • Yoshiki Akatsuka

    (Fujita Health University School of Medicine
    Aichi Cancer Center Research Institute)

  • Kazuya Shimoda

    (Faculty of Medicine, University of Miyazaki)

  • Kengo Takeuchi

    (Pathology Project for Molecular Targets, Cancer Institute, Japanese Foundation for Cancer Research)

  • Tsukasa Seya

    (Graduate School of Medicine, Hokkaido University)

  • Satoru Miyano

    (Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo)

  • Seishi Ogawa

    (Graduate School of Medicine, Kyoto University)

Abstract

Structural variations disrupting the 3′ region of PD-L1 are shown to aid immune evasion in a number of human cancers, including adult T-cell leukaemia/lymphoma, and in a mouse tumour model, CRISPR/Cas9-mediated deletion of the 3'-UTR of Pd-l1 is also shown to result in immune escape, suggesting that PD-L1 3′-UTR disruption could provide a diagnostic marker to identify patients who will benefit from anti-PD-1/PD-L1 therapy.

Suggested Citation

  • Keisuke Kataoka & Yuichi Shiraishi & Yohei Takeda & Seiji Sakata & Misako Matsumoto & Seiji Nagano & Takuya Maeda & Yasunobu Nagata & Akira Kitanaka & Seiya Mizuno & Hiroko Tanaka & Kenichi Chiba & Sa, 2016. "Aberrant PD-L1 expression through 3′-UTR disruption in multiple cancers," Nature, Nature, vol. 534(7607), pages 402-406, June.
    • Handle: RePEc:nat:nature:v:534:y:2016:i:7607:d:10.1038_nature18294
    DOI: 10.1038/nature18294
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    Cited by:

    1. Mihoko Saito-Adachi & Natsuko Hama & Yasushi Totoki & Hiromi Nakamura & Yasuhito Arai & Fumie Hosoda & Hirofumi Rokutan & Shinichi Yachida & Mamoru Kato & Akihiko Fukagawa & Tatsuhiro Shibata, 2023. "Oncogenic structural aberration landscape in gastric cancer genomes," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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