TREC mediated oncogenesis in human immature T lymphoid malignancies preferentially involves ZFP36L2

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Balducci, Estelle | Steimlé, Thomas | Smith, Charlotte | Villarese, Patrick | Feroul, Mélanie | Payet-Bornet, Dominique | Kaltenbach, Sophie | Couronné, Lucile | Lhermitte, Ludovic | Touzart, Aurore | Dourthe, Marie-Emilie | Simonin, Mathieu | Baruchel, André | Dombret, Hervé | Ifrah, Norbert | Boissel, Nicolas | Nadel, Bertrand | Macintyre, Elizabeth | Cieslak, Agata | Asnafi, Vahid

Edité par CCSD ; BioMed Central -

International audience. The reintegration of excised signal joints resulting from human V(D)J recombination was described as a potent source of genomic instability in human lymphoid cancers. However, such molecular events have not been recurrently reported in clinical patient lymphoma/leukemia samples. Using a specifically designed NGS-capture pipeline, we here demonstrated the reintegration of T-cell receptor excision circles (TRECs) in 20/1533 (1.3%) patients with T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL). Remarkably, the reintegration of TREC recurrently targeted the tumor suppressor gene, ZFP36L2, in 17/20 samples. Thus, our data identified a new and hardly detectable mechanism of gene deregulation in lymphoid cancers providing new insights in human oncogenesis.

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