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In addition to currently defined AML subgroups, three heterogeneous genomic categories emerged: AML with mutations in genes encoding chromatin, RNA-splicing regulators, or both (in 18 of patients); AML with TP53 mutations, chromosomal aneuploidies, or both (in 13); and, provisionally, AML with IDH2 R172 mutations (in 1). Patients with chromatin‚spliceosome and TP53 ‚aneuploidy AML had poor outcomes, with the various class-defining mutations contributing independently and additively to the outcome. In addition to class-defining lesions, other co-occurring driver mutations also had a substantial effect on overall survival. The prognostic effects of individual mutations were often significantly altered by the presence or absence of other driver mutations.

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