De novo activating mutations drive clonal evolution and enhance clonal fitness in KMT2A-rearranged leukemia

De novo activating mutations drive clonal evolution and enhance clonal fitness in KMT2A-rearranged leukemia

In acute leukemia with KMT2A rearrangements (KMT2A-R), activating signaling mutations are common. Here, the authors use a retroviral acute myeloid mouse leukemia model to show that subclonal de novo activating mutations drive clonal evolution in acute leukemia with KMT2A-R and enhance clonal fitness...

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Autores principales: Axel Hyrenius-Wittsten, Mattias Pilheden, Helena Sturesson, Jenny Hansson, Michael P. Walsh, Guangchun Song, Julhash U. Kazi, Jian Liu, Ramprasad Ramakrishan, Cristian Garcia-Ruiz, Stephanie Nance, Pankaj Gupta, Jinghui Zhang, Lars Rönnstrand, Anne Hultquist, James R. Downing, Karin Lindkvist-Petersson, Kajsa Paulsson, Marcus Järås, Tanja A. Gruber, Jing Ma, Anna K. Hagström-Andersson
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2018
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Science
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Acceso en línea:https://doaj.org/article/90c8b9707fb44780aabe13e7a04984b5
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Sumario:In acute leukemia with KMT2A rearrangements (KMT2A-R), activating signaling mutations are common. Here, the authors use a retroviral acute myeloid mouse leukemia model to show that subclonal de novo activating mutations drive clonal evolution in acute leukemia with KMT2A-R and enhance clonal fitness.

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