K. Okonechnikov

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.

Cellular development and evolution of the mammalian cerebellum

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

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.

Recurrent fusions in PLAGL1 define a distinct subset of pediatric-type supratentorial ependymoma

The paper identifies a novel subset of supratentorial ependymomas in children characterized by recurrent PLAGL1 fusions and distinct molecular features.

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.

Functional loss of a non-canonical BCOR-PRC1.1 complex accelerates SHH-driven medulloblastoma formation

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