Giulio Sartori

This study identifies DDX21 as a key effector of ETS1/FLI1 in ABC-DLBCL, linking it to cell cycle, immune evasion, and snoRNA processing, with potential therapeutic implications.

This study identifies IL-16 production as a mechanism of resistance to BTK inhibitors and R-CHOP in lymphomas, showing that targeting the IL-16/CD9 axis restores drug sensitivity.

This study identifies multiple resistance mechanisms to ETS-targeting agents in DLBCL and suggests combination therapies with BCL2, MCL1, and XPO1 inhibitors.

This study shows that combining infigratinib with BTK/PI3K inhibitors or bendamustine improves efficacy in lymphoma cell models, reversing resistance and suggesting FGFR inhibition as a therapeutic strategy.

This study identifies PLK1 inhibition as a strategy to enhance BTK blockade in MZL by overcoming resistance through transcriptomic and mechanistic analysis.

This study identifies HERV-K as a therapeutic target in DLBCL, develops a humanized nanobody with anti-lymphoma activity, and shows its potential through antibody-dependent cytotoxicity.