Article
TP53 mutations and TET2 deficiency cooperate to drive leukemogenesis and establish an immunosuppressive environment.
The Journal of clinical investigation - 15 May 2025
Zhang Pu, Whipp Ethan C, Skuli Sarah J, Gharghabi Mehdi, Saygin Caner, Sher Steven A, Carroll Martin, Pan Xiangyu, Eisenmann Eric D, Lai Tzung-Huei, Harrington Bonnie K, Chan Wing Keung, Youssef Youssef, Chen Bingyi, Penson Alex, Lewis Alexander M, Castro Cynthia R, Fox Nina, Cihan Ali, Le Luduec Jean-Benoit, DeWolf Susan, Kauffman Tierney, Mims Alice S, Canfield Daniel, Phillips Hannah, Williams Katie E, Shaffer Jami, Lozanski Arletta, Doong Tzyy-Jye, Lozanski Gerard, Mao Charlene, Walker Christopher J, Blachly James S, Daniyan Anthony F, Alinari Lapo, Baiocchi Robert A, Yang Yiping, Grieselhuber Nicole R, Campbell Moray J, Baker Sharyn D, Blaser Bradley W, Abdel-Wahab Omar, Lapalombella Rosa
Abstract excerpt
Mutations and deletions in TP53 are associated with adverse outcomes in patients with myeloid malignancies, and there is an urgent need for the development of improved therapies for TP53-mutant leukemias. Here, we identified mutations in TET2 as the most common co-occurring mutation in patients with TP53-mutant acute myeloid leukemia (AML). In mice, combined hematopoietic-specific deletion of TET2 and TP53...
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