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MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers

Author

Listed:
  • Christian Steidl

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Sohrab P. Shah

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Bruce W. Woolcock

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Lixin Rui

    (Metabolism Branch, Center for Cancer Research, National Cancer Institute)

  • Masahiro Kawahara

    (Albert Einstein College of Medicine)

  • Pedro Farinha

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Nathalie A. Johnson

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Yongjun Zhao

    (Genome Sciences Centre, BC Cancer Agency)

  • Adele Telenius

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Susana Ben Neriah

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Andrew McPherson

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Barbara Meissner

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Ujunwa C. Okoye

    (Albert Einstein College of Medicine)

  • Arjan Diepstra

    (University Medical Center Groningen, University of Groningen)

  • Anke van den Berg

    (University Medical Center Groningen, University of Groningen)

  • Mark Sun

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Gillian Leung

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Steven J. Jones

    (Genome Sciences Centre, BC Cancer Agency)

  • Joseph M. Connors

    (BC Cancer Agency Centre for Lymphoid Cancer)

  • David G. Huntsman

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Kerry J. Savage

    (BC Cancer Agency Centre for Lymphoid Cancer)

  • Lisa M. Rimsza

    (University of Arizona)

  • Douglas E. Horsman

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

  • Louis M. Staudt

    (Metabolism Branch, Center for Cancer Research, National Cancer Institute)

  • Ulrich Steidl

    (Albert Einstein College of Medicine)

  • Marco A. Marra

    (Genome Sciences Centre, BC Cancer Agency
    University of British Columbia)

  • Randy D. Gascoyne

    (Centre for Lymphoid Cancers and the Centre for Translational and Applied Genomics (CTAG))

Abstract

MHC regulator in cancers Using whole transcriptome sequencing, Steidl et al. identify recurrent gene translocations in B-cell lymphomas that involve the class II transactivator CIITA, the 'master regulator' of the major histocompatibility complex. These translocations downregulate cell surface HLA class II and, with some fusion partners, lead to overexpression of CD274/CD273 ligands, potentially reducing the anti-tumour immune response against these lymphomas. Recurrent rearrangements of CIITA may represent a genetic mechanism that is involved more widely in interactions between tumours and their microenvironment in lymphoid cancers.

Suggested Citation

  • Christian Steidl & Sohrab P. Shah & Bruce W. Woolcock & Lixin Rui & Masahiro Kawahara & Pedro Farinha & Nathalie A. Johnson & Yongjun Zhao & Adele Telenius & Susana Ben Neriah & Andrew McPherson & Bar, 2011. "MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers," Nature, Nature, vol. 471(7338), pages 377-381, March.
  • Handle: RePEc:nat:nature:v:471:y:2011:i:7338:d:10.1038_nature09754
    DOI: 10.1038/nature09754
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    Cited by:

    1. Heng-Jia Liu & Heng Du & Damir Khabibullin & Mahsa Zarei & Kevin Wei & Gordon J. Freeman & David J. Kwiatkowski & Elizabeth P. Henske, 2023. "mTORC1 upregulates B7-H3/CD276 to inhibit antitumor T cells and drive tumor immune evasion," Nature Communications, Nature, vol. 14(1), pages 1-22, December.

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