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Related Concept Videos

Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...

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Related Experiment Video

Updated: May 28, 2026

Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma
09:17

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

Published on: September 13, 2022

A Vascular-Extracellular Matrix Molecular Program Identifies High-Risk Diffuse Glioma Across Independent Multi-Omics.

Shamsa Hilal Saleh1, Arshiya Akbar1, Fareeha Arshad1

  • 1College of Medicine, Alfaisal University, Riyadh 11533, Saudi Arabia.

Cancers
|May 27, 2026
PubMed
Summary
This summary is machine-generated.

A novel vascular-extracellular matrix (ECM) remodeling axis (Factor 1) is a reproducible prognostic program in diffuse gliomas. This program, associated with the tumor microenvironment, shows consistent adverse effects across patient cohorts.

Keywords:
IDH stratificationMOFAconcordance indexcross-cohort validationdiffuse gliomaglioblastomamulti-omics integrationtumor purity

Related Experiment Videos

Last Updated: May 28, 2026

Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma
09:17

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

Published on: September 13, 2022

Area of Science:

  • Oncology
  • Genomics
  • Molecular Biology

Background:

  • Gliomas exhibit significant molecular heterogeneity, complicating biomarker reproducibility due to tumor purity and IDH mutation status.
  • Immune and stromal cell contamination in bulk tumor samples can obscure intrinsic molecular signatures.

Purpose of the Study:

  • To identify intrinsic molecular signatures in diffuse gliomas using multi-omics data.
  • To assess the prognostic independence and biological significance of these signatures.
  • To validate findings across independent patient cohorts.

Main Methods:

  • Utilized MOFA+ to derive molecular signatures from transcriptional, methylation, and genomic profiles of 667 diffuse gliomas (TCGA).
  • Derived factor scores on independent Chinese Glioma Genome Atlas (CGGA) cohorts (Batch 1, n=325; Batch 2, n=693) without retraining.
  • Assessed prognostic independence via multivariable Cox regression, purity-residualized survival analysis, and IDH-stratified analyses.
  • Validated signatures using concordance index and survival extreme profiling; projected onto single-cell RNA-seq data.

Main Results:

  • MOFA+ identified 12 latent factors; a vascular-extracellular matrix (ECM) remodeling axis (Factor 1) explained the most variance (24.9%) and was the strongest independent prognostic factor.
  • Factor 1 remained independently prognostic after adjusting for IDH status, tumor purity, and other clinical variables in CGGA cohorts, showing consistent directionality but variable significance in TCGA.
  • Factor 1 demonstrated comparable discrimination to the Mesenchymal signature and outperformed other classifiers, consistently separating patients with extreme survival phenotypes.

Conclusions:

  • The vascular-ECM axis represents a reproducible, purity-robust prognostic program in diffuse glioma, with consistent adverse effects across TCGA and CGGA cohorts (n=1685).
  • Factor 1 reflects a vascular/ECM-associated tumor microenvironment ecosystem program, involving malignant cells, endothelial, and myeloid compartments.
  • While prognostic in external validation cohorts, its subgroup-specific significance is cohort-dependent; findings suggest a generalizable biological program rather than a uniformly replicated subgroup biomarker.