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Pathogenic alterations of  TP53  are an independent poor prognostic factor in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Clinical course of  TP53 - altered myeloid neoplasms is dictated by genetic characteristics, such as  TP53  allelic state and variant allele frequency (VAF), and not the blast count. Hence, it was recently proposed that MDS (with increased blasts) and AML with  TP53  alterations may be best classified as a single molecular disease entity,  TP53 -mutated higher-risk (HR)-MDS/AML.  TP53  mutations drive resistance to intensive chemotherapies and less intensive hypomethylating agents (HMA). Novel combinations incorporating BCL2 inhibitor venetoclax improve response rates for  TP53 -mutated subgroup, but the survival is not improved. Early clinical studies combining HMA with investigational agents demonstrated activity in  TP53 -mutated HR-MDS/AML, but updated results with larger samples, longer follow-up, or randomized trials were less impressive to date. Future research should focus on finding novel, potentially disease-modifying therapies to improve outcomes in patients with  TP53 -mutated HR-MDS/AML.

TP53 -altered higher-risk myelodysplastic syndromes/neoplasms and acute myeloid leukemia: a distinct genetic entity with unique unmet needs