摘要
Acute myeloid leukemia(AML)arises when hematopoietic stem or progenitor cells accumulate sufficient cancer driver events to confer a transformed phenotype,resulting in an accumulation of myeloid blast cells in the bone marrow and periphery.Prognostic stratification of AML based on karyotypic and driver mutation load has become increasingly accurate in predicting risk of relapse.^(1) In therapeutic design,the utility of genomic structure and mutation data is beginning to inform the selection of targeted agents for use during induction and consolidation therapy regimens,but the number of approved drugs is far from complete when compared to the catalog of AML genomic driver events.2,3 In parallel to efforts to identify new targeted therapeutics in AML,investigation to identify shared oncogenic properties of AMLs that are not necessarily exclusive to particular driver events may yield novel therapeutic opportunities.
