S. M. Pfister

The paper uses single-cell transcriptomics to show how two compartments in medulloblastoma are connected through a migrating precursor stage, revealing spatial and developmental links between proliferating and differentiated tumor cells.

This study identifies chr8 gains and 4E-BP1 expression as prognostic markers in Ewing sarcoma, showing they drive cancer progression by promoting proliferation and sensitizing to CDK4/6 inhibitors.

This study uses single-nucleus RNA-sequencing to compare cerebellar development across human, mouse, and opossum, revealing conserved and species-specific gene expression patterns.

The paper maps the cellular origins of three common pediatric brain tumors using a single-nucleus atlas and transcriptome data, identifying lineage-specific origins and potential therapeutic targets.

This study analyzes mutational signatures in pediatric cancers, finding fewer active signatures compared to adult cancers and linking specific signatures to TP53 mutations and chromothripsis.

This study analyzes single-cell multi-omics data from medulloblastoma to explore genomic and transcriptomic impacts of chromothripsis and its subclonal variation.

The paper identifies genetic interactions in childhood cancers using a statistical pipeline, revealing 15 co-occurring and 27 mutually exclusive gene pairs, with most mechanisms linked to tumor subtypes or pathways.

The paper develops a simplified method for isolating nuclei from frozen tumor tissues and applies it to analyze pediatric central nervous system tumors using snRNA-seq.

This study identifies a distinct subset of pediatric gliomas with EGFR alterations, H3K27me3 loss, and broad tumor localization, suggesting EGFR inhibition as a potential therapy.

This study shows that loss of BCOR in SHH-medulloblastoma accelerates tumor formation by disrupting the BCOR-PRC1.1 complex and increasing Igf2 expression.

This study analyzes mRNA signals in 1,300 kidney tumors to determine their differentiation state and origin, finding that childhood tumors show fetal signals while most adult tumors do not, with exceptions in certain cancer types.