D. T. W. Jones

Cell-state plasticity drives heterogeneity in Group 3/4 medulloblastoma

This study identifies cell-state plasticity as a driver of heterogeneity in Group 3/4 medulloblastomas, showing that transcription factor perturbation can redirect tumor cells along different differentiation trajectories.

Medulloblastoma oncogene aberrations are not involved in tumor initiation, but essential for disease progression and therapy resistance

The paper uses single-cell technologies to show that large-scale chromosomal aberrations drive medulloblastoma initiation, while single-gene oncogenic events like MYC contribute to progression and therapy resistance.

Compartments in medulloblastoma with extensive nodularity are connected through differentiation along the granular precursor lineage

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.

Mapping pediatric brain tumors to their origins in the developing cerebellum

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.

Comprehensive analysis of mutational signatures in pediatric cancers

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.

Establishment of a simplified preparation method for single-nucleus RNA-sequencing and its application to long-term frozen tumor tissues

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.

A subset of pediatric thalamic gliomas share a distinct DNA methylation profile, H3K27me3 loss and frequent alteration of EGFR

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.