Jonathan Harry Schatz

This study shows BCL10 gain-of-function mutations prevent naive B cells from entering germinal centers and cooperate with BCL6 to cause extrafollicular diffuse large B-cell lymphoma.

This paper identifies GAK as a novel mitotic kinase and therapeutic target in DLBCL, showing that GAK inhibition causes mitotic defects and that existing drugs can be repurposed for its targeting.

This study shows mitochondrial translation is sensitive to ATP synthase activity, with matrix GTP availability identified as a key constraint.

This study shows that DPP-4 inhibition improves CD8+ T cell metabolism and anti-tumor activity in preclinical and clinical settings.

This study shows that inhibiting cap-dependent translation in lymphoma cells increases sensitivity to ferroptosis and CAR-T therapy by reducing NRF2 expression.

The paper investigates the mutagenic impact of radiotherapy in hematologic malignancies and finds that RT contributes to the ID8 mutational signature, which is associated with treatment resistance and relapse.