Andrea Rinaldi

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 paper shows that CDK9 inhibitor PRT2527 kills marginal zone lymphoma cells, even those resistant to other drugs, and enhances the effects of BTK, PI3K, and BCL2 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 shows that loss of EHF promotes cell plasticity, transformation, and androgen independence in early prostate cancer by disrupting lineage integrity and activating downstream pathways.

This study evaluates the preclinical efficacy of BGB-16673 and sonrotoclax in marginal zone lymphoma models, showing enhanced apoptosis when combined.

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

This study shows that disrupting FOXA1 and FOXA2 disrupts oncogenic programs in both AR-positive and AR-negative prostate cancers.

This study identifies TRIM24 as a target for preventing prostate cancer progression by degrading it to counteract AR inhibition adaptation and tumor relapse.

This study shows that combining CXCR4 inhibitors with standard and targeted therapies improves anti-tumor effects in B-cell lymphoma models, especially in drug-resistant cases.

This paper identifies ADARreg, an elncRNA that modulates BCR signaling and immune evasion in lymphoma by altering RNA stability, localization, and editing, providing a potential therapeutic target.

This paper identifies two resistance mechanisms to the CD37-targeting ADC naratuximab emtansine in lymphoma cell lines and suggests combination therapies to overcome resistance.

This study shows that mtDNA released by senescent cells triggers immunosuppression via PMN-MDSCs, and inhibiting this pathway enhances therapy-induced senescence in cancer.