Endogenous topoisomerase II-mediated DNA breaks drive thymic cancer predisposition linked to ATM deficiency

The ATM kinase is a key regulator of the DNA damage response to double-strand breaks (DSBs) and its homozygous loss in patients predisposes to lymphoid malignancies. Here, the authors develop a Tdp2 −/− Atm −/− double-deficient mouse model to uncover topoisomerase II-induced DSBs as significant driv...

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Autores principales: Alejandro Álvarez-Quilón, José Terrón-Bautista, Irene Delgado-Sainz, Almudena Serrano-Benítez, Rocío Romero-Granados, Pedro Manuel Martínez-García, Silvia Jimeno-González, Cristina Bernal-Lozano, Cristina Quintero, Lourdes García-Quintanilla, Felipe Cortés-Ledesma
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2020
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Acceso en línea:https://doaj.org/article/9f1676662817487ea864a82ec0a5a86d
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Sumario:The ATM kinase is a key regulator of the DNA damage response to double-strand breaks (DSBs) and its homozygous loss in patients predisposes to lymphoid malignancies. Here, the authors develop a Tdp2 −/− Atm −/− double-deficient mouse model to uncover topoisomerase II-induced DSBs as significant drivers of the genomic rearrangements that underpin these tumours.