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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.

Cancer Stem Cells and Tumor Maintenance

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...

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...

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Related Experiment Video

Updated: Jan 9, 2026

Isolation and Characterization of Tumor-initiating Cells from Sarcoma Patient-derived Xenografts

Isolation and Characterization of Tumor-initiating Cells from Sarcoma Patient-derived Xenografts

Published on: June 13, 2019

Tumor-initiating stem cells engineer immunity.

Zhe Yang¹, Linheng Li²

¹Stowers Institute for Medical Research, Kansas City, MO 64110, USA.

|December 5, 2025

Summary

This summary is machine-generated.

High SOX2 cancer stem cells reprogram neutrophils, hindering immunotherapy effectiveness. These reprogrammed neutrophils maintain a pro-tumor state at the tumor-stroma interface, impacting treatment outcomes.

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Using Human Induced Pluripotent Stem Cells for the Generation of Tumor Antigen-specific T Cells

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Published on: October 24, 2019

Area of Science:

Oncology
Immunology
Cancer Stem Cell Biology

Background:

Immunotherapy effectiveness is often limited by the tumor microenvironment.
Cancer stem cells (CSCs) play a crucial role in tumor recurrence and treatment resistance.
The interaction between CSCs and immune cells within the tumor microenvironment is critical for therapeutic response.

Purpose of the Study:

To investigate how SOX2-high tumor-initiating stem cells influence the tumor microenvironment during immunotherapy.
To identify the mechanisms by which CSCs evade immune surveillance and promote tumor progression post-immunotherapy.
To understand the role of neutrophils in mediating the interaction between SOX2-high CSCs and immunotherapy.

Main Methods:

Utilized mouse models of cancer with SOX2-high tumor-initiating stem cells.
Analyzed immune cell populations, particularly neutrophils, within the tumor microenvironment before and after immunotherapy.
Investigated the molecular signaling pathways involved in SOX2-high CSC-neutrophil interactions using transcriptomic and proteomic analyses.

Main Results:

SOX2-high tumor-initiating stem cells were found to reprogram neutrophils within the tumor microenvironment.
Reprogrammed neutrophils inhibited interferon-induced anti-tumor responses crucial for immunotherapy efficacy.
These neutrophils maintained a pro-tumor phenotype at the tumor-stroma interface, supporting CSC survival and tumor growth.

Conclusions:

SOX2-high CSCs actively manipulate the tumor microenvironment by reprogramming neutrophils.
Neutrophil reprogramming by CSCs represents a significant mechanism of immunotherapy resistance.
Targeting the SOX2-high CSC-neutrophil axis could offer novel therapeutic strategies to enhance immunotherapy outcomes.