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Updated: May 15, 2026

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports
Published on: November 28, 2019
Neutralizing tumor-promoting chronic inflammation: a magic bullet?
Lisa M Coussens1, Laurence Zitvogel, A Karolina Palucka
1Department of Cell and Developmental Biology, Knight Cancer Institute, Oregon Health and Science University, Portland, OR 97239-3098, USA. coussenl@ohsu.edu
Abstract:
There have been substantial advances in cancer diagnostics and therapies in the past decade. Besides chemotherapeutic agents and radiation therapy, approaches now include targeting cancer cell-intrinsic mediators linked to genetic aberrations in cancer cells, in addition to cancer cell-extrinsic pathways, especially those regulating vascular programming of solid tumors. More recently, immunotherapeutics have entered the clinic largely on the basis of the recognition that several immune cell subsets, when chronically activated, foster tumor development. Here, we discuss clinical and experimental studies delineating protumorigenic roles for immune cell subsets that are players in cancer-associated inflammation. Some of these cells can be targeted to reprogram their function, leading to resolution, or at least neutralization, of cancer-promoting chronic inflammation, thereby facilitating cancer rejection.
Insights
Recent cancer therapies target genetic aberrations and tumor vascularization. New immunotherapeutics leverage the understanding that certain immune cells promote tumor growth, offering novel strategies to combat cancer-associated inflammation.
Area of Science:
- Oncology
- Immunology
- Cancer Research
Background:
- Cancer diagnostics and therapies have advanced significantly over the last decade.
- Current treatments include chemotherapy, radiation, targeting cancer cell-intrinsic mediators, and modulating cancer cell-extrinsic pathways.
- Immunotherapeutics have emerged, recognizing the role of chronically activated immune cells in fostering tumor development.
Purpose of the Study:
- To review clinical and experimental studies on the protumorigenic roles of immune cells in cancer-associated inflammation.
- To discuss the potential of targeting these immune cells to reprogram their function.
- To explore how reprogramming immune cells can neutralize chronic inflammation and facilitate cancer rejection.
Main Methods:
- Review of clinical studies.
- Analysis of experimental studies.
- Delineation of protumorigenic roles of immune cell subsets.
- Discussion of targeting strategies for immune cell reprogramming.
Main Results:
- Identified specific immune cell subsets that play protumorigenic roles in cancer-associated inflammation.
- Highlighted that these immune cells can be targeted to alter their function.
- Demonstrated that reprogramming these cells can resolve or neutralize cancer-promoting inflammation.
Conclusions:
- Targeting immune cell subsets involved in chronic inflammation offers a promising therapeutic strategy.
- Reprogramming these cells can lead to the resolution of cancer-promoting inflammation.
- This approach facilitates cancer rejection and improves therapeutic outcomes.
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