Florencia Cidre‐Aranaz

The paper identifies LMO7 as a fusion-regulated driver of metastasis in Ewing sarcoma using spatial transcriptomics and integrates clinical data to show its association with poor outcomes.

This study shows FET fusion proteins regulate alternative splicing in sarcomas through RNA-binding protein networks, independent of their transcriptional activity, and identifies actionable splicing targets.

This study identifies USP7 as a critical regulator of PAX3::FOXO1 enhancers in FP-RMS and shows its inhibition reduces tumor growth.

This study identifies cIAP1 as a tumor suppressor in Ewing sarcoma, showing that its re-expression inhibits proliferation and tumor growth in vitro and in vivo.

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 identifies PTPRK as a gene modulated by TMPRSS2::ERG fusion and a regulatory SNP, showing its role in prostate cancer progression and potential as a biomarker.

This paper develops a mouse model for high-risk sarcoma by delivering genetic lesions via electroporation, generating multiple sarcoma types and validating their molecular and therapeutic relevance.

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.

This study finds that high Tau expression in Ewing sarcoma cells reduces invasion and improves patient survival.

This study models EWS::FLI1 fluctuations in Ewing sarcoma, showing that partial depletion promotes metastasis and identifies gene clusters and transcription factors linked to poor prognosis.

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 improves Ewing sarcoma cell culture conditions to better reflect physiological states, revealing metabolic gene signatures linked to oncogenic fusion proteins.

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

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 presents a multi-omics cell line atlas for Ewing sarcoma, identifying new target genes and regulatory mechanisms of EWSR1-ETS fusion oncogenes.