Published September 5, 2025 | Version v1
Dataset Open

pHGGmap

Authors/Creators

  • 1. Prinses Maxima Centrum

Contributors

Contact person:

  • 1. Prinses Maxima Centrum

Description

Overview

pHGGmap is a large-scale multimodal map of pediatric-type diffuse high-grade glioma (pHGG) integrating single-cell/single-nucleus RNA sequencing (sc/snRNA-seq), single-nucleus ATAC-seq (snATAC-seq), and single-nucleus multiome (snMultiome). The resource comprises over 800,000 cells from 136 patients and captures malignant, immune, vascular, and neural/glial compartments across disease subtypes and clinical contexts. Our resource resolves in great detail malignant cell hierarchies and myeloid programs that co-structure the tumor microenvironment, and captures conserved multicellular communities that persist across clinical contexts. 

This Zenodo record provides processed gene expression (GEX) and chromatin accessibility (ATAC) data for both the discovery cohort (newly generated samples together with Jessa et al., 2022, and Liu et al., 2022) and a large validation cohort (Filbin et al., 2018; Liu et al., 2022; DeSisto et al., 2024; Sussman et al., 2024; LaBelle et al., 2025) after reference mapping onto the discovery cohort. snMultiome profiles are represented in the GEX and ATAC modalities, while preserving identical cell barcodes to enable direct matching of the assays measured in the same cell. All objects contain quality-controlled cells, harmonized annotations, and clinical metadata.

Data are shared in multiple formats to support a broad range of users: interactive Loupe Browser files for rapid exploration; Seurat/Signac R objects and AnnData (.h5ad) objects for computational analysis; filtered raw count matrices; per-cell metadata tables; and ATAC fragment files with tabix indices for reprocessing and visualization. Together, these files enable reproducible interrogation of cancer cell programs, myeloid immunomodulatory states, epigenetic regulation, and multicellular communities described in the pHGGmap study.

If you use these data, please cite:

Ruiz-Moreno C., Collot R., et al. Cancer-myeloid cell invasive program in pediatric-type diffuse high-grade glioma. bioRxiv (2026)

(When the peer-reviewed version is available, please cite that version instead.)

Abstract

Pediatric-type diffuse high-grade gliomas (pHGGs) are highly aggressive brain tumors with no effective therapies. Limited understanding of their tumor microenvironment has hindered the identification of targetable cell-cell dependencies driving tumor growth. Here, we generate pHGGmap, an integrative multimodal atlas of over 800,000 cells from 136 patients profiled across single-cell transcriptomic, epigenomic, and spatial modalities. We identify novel cancer cell states defined by developmental and context-responsive programs and uncover robust cancer-myeloid interactions that organize the tumor ecosystem. Distinct myeloid immunomodulatory programs align with specific cancer cell states, revealing three conserved multicellular niches across patients and treatment. One conserved stem-like-enriched niche couples disseminating radial glial-like (RG-like) cancer cells with complement-enriched macrophages, indicative of cellular co-option supporting invasion. Longitudinal profiling of a metastatic pHGG case further supports RG-like cells as the dominant disseminating population and demonstrates a preserved association with complement-enriched macrophages even outside the brain. Our findings highlight a stable cancer-myeloid dependency and therapeutic vulnerability. Importantly, therapeutic reprogramming of this niche restores immune activation and promotes targeting of highly invasive RG-like cells. Together, pHGGmap reveals targetable cancer-myeloid dependencies in pHGG and provides a foundation for translational discovery.

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