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- W2618767609 abstract "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." @default.
- W2618767609 created "2017-06-05" @default.
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- W2618767609 date "2017-05-23" @default.
- W2618767609 modified "2023-10-11" @default.
- W2618767609 title "Cis-perturbation of cancer drivers by the HTLV-1/BLV proviruses is an early determinant of leukemogenesis" @default.
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- W2618767609 doi "https://doi.org/10.1038/ncomms15264" @default.
- W2618767609 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5457497" @default.
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- W2618767609 hasPublicationYear "2017" @default.
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