PRDM16 expression is an independent prognostic factor in AML with the double-mutant NPM1/FLT3-ITD genotype.

Generally, there was a notable trend of increasing rates of mutations interfering with active DNA-demethylation ( TET2 ; IDH1 / 2 ) with decreasing PRDM16 expression: PRDM16 High (25%), PRDM16 Int−II (34%), PRDM16 Int−I (54%), PRDM16 Low (88%) (Fig. 1 C).

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Similarly, there was a trend for even longer OS (median OS; 75.2 vs 11 months; p = 0.0561) for PRDM16 Low within AML patients with the triple-mutant NPM1 / DNMT3A / FLT3 -ITD (n = 114), but did not reach statistical significance due to the overall low number of PRDM16 Low AML patients (n = 13) in this specific subgroup (Fig. 2 E and F ).

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Therefore, an overall trend for adverse outcome in NPM1 -mutant AMLs with PRDM16 overexpression may be an epiphenomenon, reflecting the underlying genetic features rather than an independent driver of AML pathogenesis.

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