Davide Maestri

This study shows that NAD metabolism supports CTCF-cohesin chromatin regulation in EBV-transformed B-cells and identifies NAMPT inhibition as a potential therapeutic strategy.

This study identifies JunB as a key dependency factor in EBV-infected B cells that represses p18INK4c, revealing a potential therapeutic target for EBV-associated cancers.

The paper investigates the effects of decitabine on EBV-associated gastric cancer by integrating transcriptomic and methylome data, revealing retinoic acid pathway activation as a potential therapeutic target.

This study shows lamin A/C maintains genome structure and transcriptional programs needed for EBV-driven B cell activation, with loss causing chromatin reorganization and gene expression changes.

This study identifies viral lncRNAs that regulate EBV reactivation by interacting with CTCF and modulating enhancer-promoter looping.

This study shows H2A.Z.1 works with EBNA1 to maintain EBV latency by regulating chromatin structure and gene expression.

This study identifies LMP1-driven metabolic reprogramming in B-cells, showing that IMPDH inhibition sensitizes EBV-transformed cells to apoptosis, suggesting therapeutic targets for LMP1-driven lymphomas.

This study shows that WAPL suppresses LMP1 and LMP2A expression in EBV latency I by altering DNA looping and histone marks, preventing the transition to latency II.