The molecular and biological heterogeneity of AML poses significant challenges to the discovery of novel agents and therapeutic positioning. Currently, researchers utilize cell lines as ex vivo models to discover novel compounds. Additionally, investigators have coupled genomic and transcriptomic profiling in hopes of further enhancing the reliability and accuracy of these cellular models. However, cell lines often harbor strong driver alterations (e.g., KMT2A rearrangements, TP53 mutations) that occur in only a small subpopulation of AML cases. Thus, current AML cell lines may not accurately predict agent sensitivity for most patients. Here we utilize proteomics to discover new cell models that better represent AML patient biology.

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