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Updated: May 14, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

Microglia Reprogramming in Glioblastoma: Stem Cell-Derived Factors as Emerging Immunomodulators.

Zahra Amiri¹, Beatrice Federica Tremonti¹, Alessandro Corsaro¹

¹Section of Pharmacology, Department of Internal Medicine, University of Genova, Viale Benedetto XV, 2, 16132 Genova, Italy.

|May 13, 2026

Summary

Tumor-associated macrophages (TAMs) in glioblastoma resist therapies by adopting distinct states driven by metabolic and epigenetic changes. Understanding these mechanisms is crucial for developing effective glioblastoma treatments.

Keywords:

epigenetic reprogramming extracellular vesicles glioblastoma immunosuppression metabolic reprogramming microglia reprogramming potency assays stem cell secretome tumor microenvironment tumor-associated macrophages

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Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

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Last Updated: May 14, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

Area of Science:

Neuro-oncology
Cancer immunology
Cellular and molecular biology

Background:

Glioblastoma (GBM) is a challenging cancer due to cellular heterogeneity and adaptive resistance.
Current targeted therapies and immunotherapies show limited efficacy in GBM's immunosuppressive tumor microenvironment.
Tumor-associated macrophages (TAMs) play a critical role in GBM's resistance to treatment.

Purpose of the Study:

To investigate the distinct spatial and transcriptional states of TAMs in GBM.
To elucidate the mechanisms, including metabolic rewiring and epigenetic imprinting, that drive TAM immunosuppressive functions.
To identify translational challenges and propose a framework for improving immunotherapeutic strategies.

Main Methods:

Analysis of TAM states within the GBM tumor microenvironment.
Investigation of metabolic pathways (glycolysis, lactate signaling, lipid metabolism) influencing TAM function.
Examination of epigenetic modifications (DNA methylation, histone modifications) in TAMs.
Evaluation of extracellular vesicles (EVs) and stem cell secretomes as regulatory inputs.

Main Results:

TAMs exhibit a non-binary continuum of states shaped by tumor signals and niche constraints.
Metabolic rewiring and epigenetic imprinting stabilize immunosuppressive TAM phenotypes, promoting therapeutic resistance.
Extracellular vesicles and stem cell secretomes can modulate microglial regulatory control.

Conclusions:

TAMs are key drivers of glioblastoma's resistance to immune and pharmaceutical therapies.
Targeting TAM metabolic and epigenetic programs presents a potential therapeutic strategy.
An exposure-aware framework is needed to address translational confounders for effective immunotherapies.