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Epigenomic evolution in diffuse large B-cell lymphomas

Author

Listed:
  • Heng Pan

    (Institute for Computational Biomedicine, Weill Cornell Medical College
    Institute for Precision Medicine, Weill Cornell Medical College)

  • Yanwen Jiang

    (Institute for Computational Biomedicine, Weill Cornell Medical College
    Institute for Precision Medicine, Weill Cornell Medical College
    Weill Cornell Medical College)

  • Michela Boi

    (Weill Cornell Medical College
    University of Torino)

  • Fabrizio Tabbò

    (Weill Cornell Medical College
    University of Torino)

  • David Redmond

    (Institute for Computational Biomedicine, Weill Cornell Medical College
    Institute for Precision Medicine, Weill Cornell Medical College)

  • Kui Nie

    (Weill Cornell Medical College)

  • Marco Ladetto

    (Azienda Ospedaliera Santi Antonio e Biagio e Cesare Arrigo)

  • Annalisa Chiappella

    (Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino)

  • Leandro Cerchietti

    (Weill Cornell Medical College)

  • Rita Shaknovich

    (Weill Cornell Medical College)

  • Ari M. Melnick

    (Institute for Computational Biomedicine, Weill Cornell Medical College
    Weill Cornell Medical College)

  • Giorgio G. Inghirami

    (Weill Cornell Medical College
    University of Torino)

  • Wayne Tam

    (Weill Cornell Medical College)

  • Olivier Elemento

    (Institute for Computational Biomedicine, Weill Cornell Medical College
    Institute for Precision Medicine, Weill Cornell Medical College)

Abstract

The contribution of epigenomic alterations to tumour progression and relapse is not well characterized. Here we characterize an association between disease progression and DNA methylation in diffuse large B-cell lymphoma (DLBCL). By profiling genome-wide DNA methylation at single-base pair resolution in thirteen DLBCL diagnosis–relapse sample pairs, we show that DLBCL patients exhibit heterogeneous evolution of tumour methylomes during relapse. We identify differentially methylated regulatory elements and determine a relapse-associated methylation signature converging on key pathways such as transforming growth factor-β (TGF-β) receptor activity. We also observe decreased intra-tumour methylation heterogeneity from diagnosis to relapsed tumour samples. Relapse-free patients display lower intra-tumour methylation heterogeneity at diagnosis compared with relapsed patients in an independent validation cohort. Furthermore, intra-tumour methylation heterogeneity is predictive of time to relapse. Therefore, we propose that epigenomic heterogeneity may support or drive the relapse phenotype and can be used to predict DLBCL relapse.

Suggested Citation

  • Heng Pan & Yanwen Jiang & Michela Boi & Fabrizio Tabbò & David Redmond & Kui Nie & Marco Ladetto & Annalisa Chiappella & Leandro Cerchietti & Rita Shaknovich & Ari M. Melnick & Giorgio G. Inghirami & , 2015. "Epigenomic evolution in diffuse large B-cell lymphomas," Nature Communications, Nature, vol. 6(1), pages 1-12, November.
  • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7921
    DOI: 10.1038/ncomms7921
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    Cited by:

    1. Julien Broséus & Sébastien Hergalant & Julia Vogt & Eugen Tausch & Markus Kreuz & Anja Mottok & Christof Schneider & Caroline Dartigeas & Damien Roos-Weil & Anne Quinquenel & Charline Moulin & German , 2023. "Molecular characterization of Richter syndrome identifies de novo diffuse large B-cell lymphomas with poor prognosis," Nature Communications, Nature, vol. 14(1), pages 1-19, December.

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