Genomic Landscapes and Clonality of De Novo AML

Abstract

To the Editor: In reviewing the analysis of the genomic and epigenomic landscapes of de novo acute myeloid leukemia (AML) by the Cancer Genome Atlas Research Network (May 30 issue),1 we were struck by an apparent discrepancy in the reported clonal architecture of the AML samples as compared with that reported by Ding et al.2 (an average of one to two distinct clones identified vs. four or more). This discrepancy may reflect the limited depth of the sequencing analysis performed in the more recent study.1 More important, the authors do not reveal which mutations occur in the founding clone, as . . .