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Relapse in acute myeloid leukemia (AML) patients remains a clinical challenge. The majority of AML patients who receive induction treatment with combination chemotherapy achieve clinicopathologic remission. However, a significant proportion of these patients will relapse and succumb to chemoresistant disease [1]. The biological mechanisms that contribute to relapsed AML are yet to be fully deciphered. Previous studies investigating genetic contributions to AML disease relapse included small numbers of patient samples and/or focused on a small number of AML subtypes. These studies have suggested that disease relapse is associated with founder clone recurrence, subclonal expansion and/or the occurrence of relapse-specific events (reviewed in [2]). To better understand the somatic genomic changes that drive AML relapse, we analyzed specimens (n= 120) from a clinically annotated adult relapsed AML patient cohort [3] (Supplementary Table S1, Supplementary Fig. S1) for somatic events. The median age of the patient cohort was 50 years. All patients received standard of care combination chemotherapy, achieved complete remission and experienced disease relapse. We first reanalyzed whole exome sequencing (diagnosis, relapse and matched germlines) of 49 patients [3] in order to capture the complete intragenic mutational burden (Fig. 1A, Supplementary Tables S2 and S3). 21 patients had at least one mutation lost at relapse. Twenty-three patients gained at least one mutation at relapse. A subset of recurrent somatic These authors contributed equally: Ross L. Levine, Ari Melnick

Genomic and evolutionary portraits of disease relapse in acute myeloid leukemia