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Almost a decade ago, Gilliland proposed a model of leukemogenesis for acute myeloid leukemia (AML).1 In this model, AML results from activating mutations in genes that confer increased proliferation and survival capabilities (class I mutations) acting in concert with chromosomal abnormalities or gene mutations that block differentiation and subsequent apoptosis (class II mutations). In this issue of Blood, Bachas and colleagues present data that clearly demonstrate mutational shifts in class I/II genes that occur between diagnosis and relapse in children with AML.2 The authors suggest that these findings may allow for personalized treatment.

Original publication




Journal article



Publication Date





2622 - 2623