Defining a Distinct Subtype of TP53-Mutated AML via BAP1 Loss: Implications for Targeted Therapy with BCL-xL Inhibitors
Loss of the tumor suppressor BAP1 characterizes a unique subtype of TP53-mutated de novo acute myeloid leukemia (AML), correlating with poorer prognosis and erythroid lineage priming, while revealing vulnerability to BCL-xL inhibition as a promising therapeutic strategy.