Mark J. Levis

This paper develops an anti-CCRL2 antibody-drug conjugate (ADC) that shows potent cytotoxicity against high-risk MDS/AML cells without harming healthy hematopoietic cells.

This study identifies CCRL2 as a driver of IFN-γ signaling in TP53-mutated AML with erythroid differentiation, linking it to disease progression and poor outcomes.