Molecular Minimal Residual Disease Monitoring in Acute Myeloid Leukemia  Adrian G. Selim, Andrew S. Moore  The Journal of Molecular Diagnostics  Volume 20, Issue 4, Pages 389-397 (July 2018) DOI: 10.1016/j.jmoldx.2018.03.005 Copyright © 2018 American Society for Investigative Pathology and the Association for Molecular Pathology Terms and Conditions

Figure 1 Over time, hematopoietic stem/progenitor cells (HSPC) acquire passenger mutations, most of which are benign and may be found in mature progeny. Later, this HSPC acquires a leukemia-initiating mutation. If this initiating/early driver mutation commonly exists in a pre-leukemic state (such as DNMT3A mutations), the mutation may potentially be present in mature progeny. The progenitor acquires further co-operating mutations, as well as passenger mutations, which gives rise to the founding AML clone. Subsequent co-operating and passenger mutations occur in subsets of leukemic cells, giving rise to subclones (1 and 2). Thus, suitable mutations for minimal residual disease monitoring are those that are acquired between the leukemia-initiating event and the emergence of the founding clone (with the exception of mutations commonly present in the pre-leukemic state). Adapted from Welch et al,2 with permission from Elsevier. The Journal of Molecular Diagnostics 2018 20, 389-397DOI: (10.1016/j.jmoldx.2018.03.005) Copyright © 2018 American Society for Investigative Pathology and the Association for Molecular Pathology Terms and Conditions