Article
DNMT3A mutations promote anthracycline resistance in acute myeloid leukemia via impaired nucleosome remodeling.
Nature medicine - 1 Dec 2016
Guryanova Olga A, Shank Kaitlyn, Spitzer Barbara, Luciani Luisa, Koche Richard P, Garrett-Bakelman Francine E, Ganzel Chezi, Durham Benjamin H, Mohanty Abhinita, Hoermann Gregor, Rivera Sharon A, Chramiec Alan G, Pronier Elodie, Bastian Lennart, Keller Matthew D, Tovbin Daniel, Loizou Evangelia, Weinstein Abby R, Gonzalez Adriana Rodriguez, Lieu Yen K, Rowe Jacob M, Pastore Friederike, McKenney Anna Sophia, Krivtsov Andrei V, Sperr Wolfgang R, Cross Justin R, Mason Christopher E, Tallman Martin S, Arcila Maria E, Abdel-Wahab Omar, Armstrong Scott A, Kubicek Stefan, Staber Philipp B, Gönen Mithat, Paietta Elisabeth M, Melnick Ari M, Nimer Stephen D, Mukherjee Siddhartha, Levine Ross L
Abstract excerpt
Although the majority of patients with acute myeloid leukemia (AML) initially respond to chemotherapy, many of them subsequently relapse, and the mechanistic basis for AML persistence following chemotherapy has not been determined. Recurrent somatic mutations in DNA methyltransferase 3A (DNMT3A), most frequently at arginine 882 (DNMT3AR882), have been observed in AML and in individuals with clonal hematopoiesis...
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