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Cis-perturbation of cancer drivers by the HTLV-1/BLV proviruses is an early determinant of leukemogenesis

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  • Nicolas Rosewick

    (Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
    Laboratory of Experimental Hematology, Institut Jules Bordet, Université Libre de Bruxelles (ULB))

  • Keith Durkin

    (Unit of Animal Genomics, GIGA-R, Université de Liège (ULg))

  • Maria Artesi

    (Unit of Animal Genomics, GIGA-R, Université de Liège (ULg))

  • Ambroise Marçais

    (Service d’hématologie, Hôpital Universitaire Necker, Université René Descartes, Assistance publique hôpitaux de Paris)

  • Vincent Hahaut

    (Unit of Animal Genomics, GIGA-R, Université de Liège (ULg))

  • Philip Griebel

    (Vaccine and Infectious Disease Organization, VIDO-Intervac, University of Saskatchewan)

  • Natasa Arsic

    (Vaccine and Infectious Disease Organization, VIDO-Intervac, University of Saskatchewan)

  • Véronique Avettand-Fenoel

    (Laboratoire de Virologie, AP-HP, Hôpital Necker-Enfants Malades, Université Paris Descartes)

  • Arsène Burny

    (Laboratory of Experimental Hematology, Institut Jules Bordet, Université Libre de Bruxelles (ULB))

  • Carole Charlier

    (Unit of Animal Genomics, GIGA-R, Université de Liège (ULg))

  • Olivier Hermine

    (Service d’hématologie, Hôpital Universitaire Necker, Université René Descartes, Assistance publique hôpitaux de Paris
    INSERM U1163-ERL8254, Institut Imagine)

  • Michel Georges

    (Unit of Animal Genomics, GIGA-R, Université de Liège (ULg))

  • Anne Van den Broeke

    (Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
    Laboratory of Experimental Hematology, Institut Jules Bordet, Université Libre de Bruxelles (ULB))

Abstract

Human T-cell leukaemia virus type-1 (HTLV-1) and bovine leukaemia virus (BLV) infect T- and B-lymphocytes, respectively, provoking a polyclonal expansion that will evolve into an aggressive monoclonal leukaemia in ∼5% of individuals following a protracted latency period. It is generally assumed that early oncogenic changes are largely dependent on virus-encoded products, especially TAX and HBZ, while progression to acute leukaemia/lymphoma involves somatic mutations, yet that both are independent of proviral integration site that has been found to be very variable between tumours. Here, we show that HTLV-1/BLV proviruses are integrated near cancer drivers which they affect either by provirus-dependent transcription termination or as a result of viral antisense RNA-dependent cis-perturbation. The same pattern is observed at polyclonal non-malignant stages, indicating that provirus-dependent host gene perturbation contributes to the initial selection of the multiple clones characterizing the asymptomatic stage, requiring additional alterations in the clone that will evolve into full-blown leukaemia/lymphoma.

Suggested Citation

  • Nicolas Rosewick & Keith Durkin & Maria Artesi & Ambroise Marçais & Vincent Hahaut & Philip Griebel & Natasa Arsic & Véronique Avettand-Fenoel & Arsène Burny & Carole Charlier & Olivier Hermine & Mich, 2017. "Cis-perturbation of cancer drivers by the HTLV-1/BLV proviruses is an early determinant of leukemogenesis," Nature Communications, Nature, vol. 8(1), pages 1-15, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15264
    DOI: 10.1038/ncomms15264
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