Pablo Domizi

This study identifies IKAROS as a factor associated with antigen escape in B-ALL, showing that low IKAROS levels lead to reduced B-cell antigen expression and resistance to CD19- and CD22-targeted therapies.

This study identifies uridine metabolism as a therapeutic target for chemo-resistant B-ALL by linking active signaling to uridine dependency and demonstrating DHODH inhibition as a promising treatment.

The paper uses a CRISPR-based screen in 3T3-L1 cells to identify regulators of adipogenesis, finding that protein translation and stability mechanisms are critical for adipocyte expansion and lipogenesis.