Non-coding mutations drive persistence of a founder pre-leukemic clone which initiates late relapse in T-ALL

David O’Connor,Jose Espejo Valle-Inclán,Lucia Conde, Gianna Bloye,Sunniyat Rahman,Joana Costa,Jack Bartram,Stuart Adams,Gary Wright, Hilary Elrick, Kerry Wall, Sara Dyer, Christopher Howell, Galina Jigoulina,Javier Herrero,Isidro Cortes-Ciriano,Anthony V. Moorman,Marc R. Mansour

Blood（2024）

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摘要

1.Late relapse of T-ALL represents evolution of a pre-leukemic clone harbouring a single non-coding driver event that has evaded frontline chemotherapy.2.Late relapse cases are enriched for non-coding lesions driving overexpression of LMO2 and TAL1, which act as the founder events in leukemogenesis

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