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Related Concept Videos

The Tumor Microenvironment02:17

The Tumor Microenvironment

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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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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Tumor Immunotherapy01:27

Tumor Immunotherapy

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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.
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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Related Experiment Video

Updated: Jan 13, 2026

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports
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Tumor-Immune Cell Crosstalk Drives Immune Cell Reprogramming Towards a Pro-Tumor Proliferative State Involving STAT3

Karen Norek1, Jacob Kennard1, Kenneth Fuh1

  • 1Syantra Inc., 32 Royal Vista Drive NW, Suite 105, Calgary, AB T3R 0H9, Canada.

Cancers
|January 10, 2026
PubMed
Summary
This summary is machine-generated.

Cancer cells reprogram immune cells, promoting tumor growth. Inhibiting STAT3 signaling can reverse this immune cell transformation, offering a new therapeutic strategy for cancer treatment.

Keywords:
RNAseqSTAT3 inhibitionTHP1TNBCbiomarkersbreast cancercancer-immune crosstalkco-culturehuman monocytesimmune reprogrammingliquid biopsytumor microenvironmenttumor-education

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Tumor-induced immune reprogramming is a key cancer mechanism for immune evasion and disease progression.
  • The tumor microenvironment (TME) facilitates cancer metastasis and immune evasion through immune cell modulation.
  • Understanding tumor-immune cell interactions is crucial for developing novel cancer therapies.

Purpose of the Study:

  • To investigate the effects of triple-negative breast cancer (TNBC) cells on monocyte phenotype and function.
  • To identify the signaling pathways involved in tumor-induced immune cell reprogramming.
  • To evaluate the therapeutic potential of targeting these pathways for cancer treatment.

Main Methods:

  • Co-culture models using THP1 monocytes and TNBC cell lines (MDA-MB-231, BT-549).
  • Exposure of monocytes to cancer cells directly or indirectly via tumor-conditioned media.
  • Transcriptomic and pathway analyses to assess gene expression changes.
  • Functional assays to measure monocyte proliferation and cytokine production.
  • Pharmacological inhibition of STAT3 signaling using STAT3-IN-12.

Main Results:

  • Cancer-exposed monocytes exhibited a reprogrammed phenotype with activated pro-tumorigenic pathways.
  • Elevated expression of pro-inflammatory cytokines, including IL6, was observed in monocytes.
  • Significant increase in monocyte proliferation under both direct and indirect tumor exposure.
  • STAT3 inhibitor STAT3-IN-12 effectively suppressed tumor-driven monocyte proliferation.
  • STAT3 signaling was identified as a critical mediator of immune cell transformation.

Conclusions:

  • Targeting tumor-educated transcriptional programs represents a novel immunomodulatory strategy in cancer therapy.
  • Pharmacological inhibition of STAT3 can restore immune cell homeostasis and suppress pro-tumor phenotypes.
  • This approach may complement existing cancer treatments by counteracting tumor-driven immune dysregulation.
  • The study provides insights into immune cell plasticity and identifies actionable therapeutic targets.