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Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma

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Integrative Multi-Omics Analysis Identifies an SPP1-Associated Spatial Mesenchymal-Myeloid Program in Glioblastoma.

Ying Wang¹, Dong Zhou^1,2, Zhen Hong^1,2

¹Department of Neurology, West China Hospital of Sichuan University, Chengdu 610041, China.

|June 26, 2026

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Secreted phosphoprotein 1 (SPP1) is linked to glioblastoma

Area of Science:

Neuro-oncology
Cancer biology
Immunology

Background:

Glioblastoma (GBM) exhibits significant transcriptional plasticity and a complex immune microenvironment.
Molecular drivers of tumor state transitions and immune remodeling in GBM are not fully understood.

Purpose of the Study:

To investigate the role of secreted phosphoprotein 1 (SPP1) in glioblastoma tumor microenvironment organization.
To explore SPP1's association with tumor plasticity and immune cell infiltration.

Main Methods:

Integrative multi-omics analysis including single-cell, spatial transcriptomics, and computational perturbation.
Human Protein Atlas (HPA) immunohistochemistry and CODEX spatial protein imaging.
TCGA-GBM cohort analysis for survival correlation.

Keywords:

SPP1 glioblastoma mesenchymal-like state multi-omics myeloid cells

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Last Updated: Jun 27, 2026

Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma

Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma

Published on: September 13, 2022

Main Results:

SPP1 expression correlates with myeloid cell populations and mesenchymal-like (MES-like) tumor states.
SPP1 is associated with inflammatory programs and ligand-receptor interactions (SPP1-CD44, SPP1-integrin).
Elevated SPP1 and mesenchymal signatures predict poorer survival in GBM patients.

Conclusions:

SPP1 plays a role in spatial mesenchymal-myeloid organization within the GBM microenvironment.
SPP1-associated programs may serve as biomarkers for tumor plasticity and immune remodeling.