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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...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Tumor Progression02:07

Tumor Progression

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.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

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.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...

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Related Experiment Video

Updated: Jul 12, 2026

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

In Vitro Assay to Study Tumor-macrophage Interaction

Published on: August 1, 2019

Tumor-Associated Macrophages Promote Brain Metastasis.

Chaitali Khan, Nasser M Rusan

    Biorxiv : the Preprint Server for Biology
    |July 10, 2026
    PubMed
    Summary

    Brain metastasis is poorly understood, but a new study in fruit flies shows macrophages are crucial for cancer cells to colonize the brain. Depleting macrophages significantly reduced brain metastasis, highlighting a potential therapeutic target.

    Area of Science:

    • Neuroscience
    • Oncology
    • Cell Biology

    Background:

    • Brain metastasis is a significant challenge in cancer treatment, affecting 20-40% of patients.
    • Understanding how cancer cells interact with the brain's protective barriers is crucial but limited by current models.
    • The role of tumor-associated macrophages (TAMs) in brain metastasis is not fully understood.

    Purpose of the Study:

    • To develop a genetically tractable in vivo model for studying brain metastasis.
    • To investigate the mechanisms by which tumor cells interact with and remodel brain barriers.
    • To determine the causal role of TAMs in brain metastasis colonization.

    Main Methods:

    • Utilized the adult Drosophila melanogaster brain as a model system.
    • Employed allograft transplantation of neural stem cell-derived tumors (lgl-/-).

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  • Genetically depleted tumor-associated macrophages (TAMs) to assess their role.

    • Main Results:

    • Tumors formed sheet-like invasions on the brain surface, mimicking human leptomeningeal disease.
    • The basement membrane (BM) was identified as a key barrier to parenchymal invasion.
    • Genetic depletion of TAMs significantly reduced brain metastasis, suggesting a causal role in colonization.
    • TAMs were recruited to the metastatic tumor site.

    Conclusions:

    • The study establishes a conserved, macrophage-dependent mechanism in brain metastasis.
    • The Drosophila brain provides a valuable, genetically accessible model for studying brain metastasis.
    • Targeting macrophages may offer a therapeutic strategy to prevent brain metastasis colonization.