Ana Banito

The paper evaluates multi-laboratory studies to identify promising treatments by assessing effect sizes and experimental rigor across different medical fields.

This study shows that SS18::SSX can drive transcription independently of BAF complex interaction and relies on EP300 for gene activation, suggesting new therapeutic targets for synovial sarcoma.

This study shows that inhibiting SUMOylation with TAK-981 stabilizes cBAF complexes and disrupts the SS18::SSX-driven transcriptome in synovial sarcoma, leading to tumor inhibition.

This study identifies CXADR as a driver of Ewing sarcoma metastasis and shows that targeting AKT signaling with Capivasertib enhances chemotherapy efficacy in CXADR-high tumors.

This study shows that reduced EWSR1::ETS activity in Ewing sarcoma promotes immune evasion via the tryptophan-kynurenine-AHR axis, leading to worse clinical outcomes and tumor progression.

The paper identifies CACNA2D2 as a super-enhancer-driven target of EWSR1::WT1 and demonstrates its utility as a diagnostic biomarker for DSRCT.

This study investigates how SMARCB1 loss in Epithelioid Sarcoma rewires epigenetic regulation, revealing therapeutic vulnerabilities through functional multi-omics analysis.

This study examines the epigenomic states of synovial sarcoma using multi-omics analysis, revealing a continuum of epigenomic states and identifying H3K4me3 inhibition as a potential therapeutic strategy.

This study identifies GLRX3 as a vulnerability in Ewing sarcoma driven by EWSR1::FLI1 fusion oncoproteins, showing its role in oxidative stress and iron homeostasis and potential therapeutic targeting.

The paper identifies JQ1 as a molecular glue that targets centromeres by stabilizing BRD4-CENP-B interactions, enhancing centromere cohesion and affecting cell proliferation.