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Related Concept Videos

The Tumor Microenvironment02:17

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...
The Tumor Microenvironment02:17

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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Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
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Related Experiment Video

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In Vitro Assay to Study Tumor-macrophage Interaction
08:36

In Vitro Assay to Study Tumor-macrophage Interaction

Published on: August 1, 2019

"Re-educating" tumor-associated macrophages by targeting NF-kappaB.

Thorsten Hagemann1, Toby Lawrence, Iain McNeish

  • 1Centre for Cancer and Inflammation, Institute of Cancer, Barts and The London School of Medicine and Dentistry, London EC1M 6BQ, UK. t.hagemann@qmul.ac.uk

The Journal of Experimental Medicine
|May 21, 2008
PubMed
Summary
This summary is machine-generated.

Nuclear factor kappaB (NF-kappaB) signaling drives immunosuppressive tumor-associated macrophages (TAMs) in cancer. Inhibiting NF-kappaB in TAMs reverses this, making them cytotoxic and promoting tumor regression.

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • The nuclear factor kappaB (NF-kappaB) pathway is implicated in cancer-related inflammation and tumor progression.
  • Tumor-associated macrophages (TAMs) often adopt an immunosuppressive phenotype within the tumor microenvironment.

Purpose of the Study:

  • To investigate the role of NF-kappaB in maintaining the immunosuppressive phenotype of TAMs.
  • To explore the therapeutic potential of targeting NF-kappaB signaling in TAMs for cancer treatment.

Main Methods:

  • Macrophages were polarized using interleukin (IL)-1R and MyD88, requiring IkappaB kinase beta-mediated NF-kappaB activation.
  • NF-kappaB signaling was inhibited specifically in TAMs.
  • Tumor regression and immune cell recruitment were assessed in vivo.

Main Results:

  • Inhibition of NF-kappaB in TAMs induced a switch to a cytotoxic, "classically" activated phenotype (IL-12high, MHCIIhigh, IL-10low, Arginase-1low).
  • Targeting NF-kappaB in TAMs promoted regression of advanced tumors.
  • This regression was mediated by enhanced macrophage tumoricidal activity and IL-12-dependent NK cell recruitment.

Conclusions:

  • NF-kappaB signaling is crucial for maintaining the immunosuppressive nature of TAMs.
  • Targeting NF-kappaB in TAMs represents a novel therapeutic strategy to "re-educate" macrophages, enhance anti-tumor immunity, and complement existing cancer therapies.