Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Tumor Immunotherapy

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

The Tumor Microenvironment

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a rapamycin-insensitive companion...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Inflammation-responsive liposomes co-delivering tobramycin and nitric oxide for overcoming mucus barriers against MRSA pneumonia.

Colloids and surfaces. B, Biointerfaces·2026

Same author

Delivery of TCM Monomers Using Blood Cell Membrane Coated Biomimetic Nanoparticles to Target CVD.

International journal of nanomedicine·2026

Same author

The astrocytic connectome: Gap-Junction topology beyond diffuse syncytium.

Trends in cell biology·2026

Same author

Discrete subaortic stenosis: prognostic value of the left ventricular outflow tract gradient and implications for earlier surgical intervention.

World journal of pediatrics : WJP·2026

Same author

Nonlinear associations between punishment sensitivity and problematic Internet use among adolescents: Results from cross-sectional and longitudinal analyses.

International journal of clinical and health psychology : IJCHP·2026

Same author

Aqueous extract of Solanum nigrum L. restrains colorectal cancer progression by blocking cancer-associated fibroblast-induced STAT3-Annexin A2 signaling.

Phytomedicine : international journal of phytotherapy and phytopharmacology·2026

Search research articles

Related Experiment Video

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

Astrocyte-associated immunosuppressive programs in brain tumors: a STAT3-centered perspective.

Wei Sun^1,2, Jia-Qi Zhang³, Wei-Lin Jin⁴

¹Department of Neurosurgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.

Cancer Metastasis Reviews

|May 13, 2026

Summary

Astrocytes create immunosuppressive tumor microenvironments in brain cancers. Targeting these astrocyte-centered hubs (MISH) may reprogram them to enhance immunotherapy effectiveness.

Keywords:

Astrocyte Brain metastases Cell signaling Cell-cell communication Glioblastoma Immunosuppression STAT3 Tumor microenvironment

More Related Videos

Delivery of Antibodies into the Murine Brain via Convection-enhanced Delivery

Delivery of Antibodies into the Murine Brain via Convection-enhanced Delivery

Published on: July 18, 2019

Related Experiment Videos

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

Delivery of Antibodies into the Murine Brain via Convection-enhanced Delivery

Delivery of Antibodies into the Murine Brain via Convection-enhanced Delivery

Published on: July 18, 2019

Area of Science:

Neuro-oncology
Immunology
Cancer Biology

Background:

Astrocytes are key players in the immunosuppressive tumor microenvironment (TME) of brain tumors like glioblastoma.
Tumor-associated astrocytes (TAAs) interact with tumor cells, myeloid cells, and vasculature to impair local immune responses.

Purpose of the Study:

To introduce the concept of modular immunosuppressive hubs (MISH) centered on astrocytes.
To provide a framework for understanding astrocyte-driven immunosuppression in brain tumors, focusing on STAT3 signaling.
To highlight therapeutic strategies targeting MISH for improved immunotherapy outcomes.

Main Methods:

Systematic deconstruction of MISH composition, spatial regulation, and signaling.
Analysis of cell-cell communication networks within the TME.
Review of emerging pharmacological strategies targeting MISH signaling pathways.

Main Results:

MISH represent organized suppressive programs within tumor niches, mediated by astrocyte interactions.
STAT3-centered signaling is a critical component of these MISH.
Targeting MISH can disrupt astrocyte-mediated immunosuppression.

Conclusions:

Astrocytes actively shape the immunosuppressive TME through MISH.
Dismantling MISH by targeting specific signaling pathways offers a novel therapeutic approach.
Reprogramming TAAs via MISH targeting could overcome immunotherapy resistance in brain tumors.