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The clinical and molecular spectrum of acute myeloid leukemia (AML) is highly complex, with specific chromosomal and genetic biomarkers correlating with patient response to treatment and survival. Now, to better understand the genetics of AML and the implications for therapy and prognosis, investigators conducted a multiplatform, genomic and epigenomic analysis of 200 clinically annotated adult de novo AML samples collected at a single institution.
A total of 260 genes were mutated in ≥2 samples; 23 of these were mutated at a higher-than-expected frequency. Abnormalities included coding-sequence mutations and gene fusions as well as epigenomic anomalies in DNA methylation and miRNA expression. Dysregulated pathways encompassed transcription …