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Secondary ontogeny mutations in patients with acute myeloid leukemia (AML) are associated with adverse risk and poor survival outcomes.1 However, whether secondary mutations confer a poor prognosis with hypomethylating agents (HMA) + venetoclax (Ven) compared with HMA monotherapy is unknown.1
Here, we summarize results from a retrospective study by Shimony et al.1 published in Leukemia, evaluating whether secondary molecular ontogeny implies adverse risk in patients with AML treated with HMA + Ven. Also investigated was the benefit of adding Ven to HMA monotherapy by ontogeny group.
Figure 1. Median OS of patients with de novo, secondary, or TP53 mutated disease treated with HMA + Ven or HMA monotherapy*
HMA, hypomethylating agent; OS, overall survival; Ven, venetoclax.
*Adapted from Shimony, et al.1
†HMA + Ven (n = 38) and HMA monotherapy (n = 50).
‡HMA + Ven (n = 68) and HMA monotherapy (n = 47).
§HMA + Ven (n = 60) and HMA monotherapy (n = 51).
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