Olivier Delattre

The paper shows EWSR1::FLI1 fusion drives the production of cancer-specific neoproteins in Ewing sarcoma, revealing a reversible dark proteome with therapeutic potential.

The paper demonstrates that TCR-T cells targeting neogene-encoded antigens can specifically kill Ewing sarcoma cells in vitro and in vivo.

The paper introduces a PDX platform for pediatric cancers, providing in vivo drug testing models and molecular data to aid in therapy development.

This study identifies 14 susceptibility loci for Ewing sarcoma through a genome-wide association meta-analysis, revealing genetic interactions with somatic EWSR1::FLI1 fusions.

This paper develops a label-free platform combining microfluidics, morphological analysis, and machine learning to predict chemotherapy effects on tumor spheroids, showing robust performance across cell lines and patient-derived samples.

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 compares genomic and phenotypic stability of pediatric Ewing sarcoma cell lines to adult carcinoma cell lines over 12 months of culture.

The paper uses single-cell RNA sequencing to show that the mouse pelvic ganglion contains neurons distinct from both sympathetic and parasympathetic types, and that pelvic organs are innervated by a divergent sympathetic pathway, not parasympathetic or typical sympathetic neurons.

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

transmorph provides a flexible framework for single-cell data integration, enabling complex pipelines and demonstrating its utility in various integration tasks.

The paper introduces QuantumClone, a method for clonal reconstruction in cancer that accounts for variant allele frequencies and genotypes, and applies it to neuroblastoma samples to identify recurrently altered pathways in different clonal populations.