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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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Related Experiment Video

Updated: Jun 23, 2026

Murine Experimental Model of Original Tumor Development and Peritoneal Metastasis via Orthotopic Inoculation with Ovarian Carcinoma Cells

Murine Experimental Model of Original Tumor Development and Peritoneal Metastasis via Orthotopic Inoculation with Ovarian Carcinoma Cells

Published on: December 9, 2016

Epithelial tumors: Growing from within.

Mariana Muzzopappa¹, Marco Milán^1,2

¹a Institute for Research in Biomedicine (IRB Barcelona) , the Barcelona Institute of Science and Technology , Baldiri Reixac, 10-12, Barcelona , Spain.

|February 17, 2018

Summary

Tumor growth can be driven by internal cell interactions, independent of external signals. This mechanism, involving distinct tumor cell populations activating the JNK pathway, contributes to unlimited tumor potential.

Keywords:

Chromosomal instability Eiger cell delamination cell polarity epithelial tumor

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Generating and Imaging Mouse and Human Epithelial Organoids from Normal and Tumor Mammary Tissue Without Passaging

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Generating and Imaging Mouse and Human Epithelial Organoids from Normal and Tumor Mammary Tissue Without Passaging

Generating and Imaging Mouse and Human Epithelial Organoids from Normal and Tumor Mammary Tissue Without Passaging

Published on: November 11, 2022

Area of Science:

Developmental Biology
Cancer Biology
Cell Signaling

Background:

Epithelial tumor growth is influenced by stromal interactions.
The TNF ligand Eiger activates the JNK pathway, promoting tumor progression.
JNK signaling drives tumor growth, invasiveness, and malignancy.

Purpose of the Study:

To review findings on a tumor-intrinsic mechanism for unlimited tumor growth.
To explore Eiger- and stroma-independent pathways.
To investigate cell-cell interactions driving tumor progression.

Main Methods:

Utilized Drosophila models to study epithelial tumors.
Minimized direct contact between tumor cells and wild-type epithelial cells.
Analyzed cell-autonomous JNK activation within distinct tumor cell populations.

Main Results:

Identified a tumor-intrinsic mechanism for unlimited growth potential.
This mechanism is independent of Eiger and stroma.
Distinct tumor cell populations activate JNK autonomously, creating feedback loops.

Conclusions:

Cell interaction-based feedback loops amplify tumor growth potential.
This newly identified mechanism contributes to malignancy.
Findings may guide targeted drug therapies for epithelial tumors.