Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia.
Wong, Terrence N; Ramsingh, Giridharan; Young, Andrew L; Miller, Christopher A; Touma, Waseem; Welch, John S; Lamprecht, Tamara L; Shen, Dong; Hundal, Jasreet; Fulton, Robert S; Heath, Sharon; Baty, Jack D; Klco, Jeffery M; Ding, Li; Mardis, Elaine R; Westervelt, Peter; DiPersio, John F; Walter, Matthew J; Graubert, Timothy A; Ley, Timothy J; Druley, Todd; Link, Daniel C; Wilson, Richard K.
; 518(7540): 552-555, 2015 Feb 26.
Artigo em Inglês | MEDLINE | ID: mdl-25487151
Identification of pre-leukaemic haematopoietic stem cells in acute leukaemia.
How One Thing Led to Another.
Relative mitochondrial priming of myeloblasts and normal HSCs determines chemotherapeutic success in AML.
Rapid expansion of preexisting nonleukemic hematopoietic clones frequently follows induction therapy for de novo AML.
The origin and evolution of mutations in acute myeloid leukemia.
The methyltransferase G9a regulates HoxA9-dependent transcription in AML.
Cancer-associated IDH2 mutants drive an acute myeloid leukemia that is susceptible to Brd4 inhibition.
BET inhibitor resistance emerges from leukaemia stem cells.
Epigenetic Abnormalities in Acute Myeloid Leukemia and Leukemia Stem Cells.
DNA Damage Response in Quiescent Hematopoietic Stem Cells and Leukemia Stem Cells.