Michael Andreeff

This study uses spatial proteomics to reveal that TP53 mutant AML residual disease forms immunosuppressive niches in the bone marrow, segregated from T-cells, suggesting niche-level immune evasion.

This study identifies that macrophage-secreted pyrimidine metabolites confer chemotherapy resistance in AML by inhibiting drug activation, and shows that targeting macrophage metabolism can restore drug sensitivity.

This study identifies BIRC5 as a targetable vulnerability in TP53 mutant AML, showing that survivin/IAP inhibitors can overcome therapy resistance.

This paper identifies a novel MYC-GSPT1 feedback loop and reports a dual degrader, GT19630, that effectively targets MYC-driven cancers with anti-proliferative and apoptotic effects.

The paper quantifies the impact of TP53 mutations in myelodysplastic syndromes using an evolutionary action score and correlates it with clinical and genomic features, finding that low-EAp53 mutations are associated with better survival.