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The Tumor Microenvironment

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 Microenvironment

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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Related Experiment Video

Updated: May 20, 2026

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Published on: May 17, 2024

The plexiform neurofibroma microenvironment.

Feng-Chun Yang¹, Karl Staser, D Wade Clapp

¹Herman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA, fyang@iupui.edu.

Cancer Microenvironment : Official Journal of the International Cancer Microenvironment Society

|July 24, 2012

Summary

This summary is machine-generated.

Tumor-stromal interactions drive plexiform neurofibromas in Neurofibromatosis type 1 (NF1). Targeting the stem cell factor/c-kit pathway offers a promising therapeutic strategy for these NF1 tumors.

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An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas

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Last Updated: May 20, 2026

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Identifying, Diagnosing, and Grading Malignant Peripheral Nerve Sheath Tumors in Genetically Engineered Mouse Models

Published on: May 17, 2024

An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas

An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas

Published on: October 10, 2025

Area of Science:

Oncology
Genetics
Immunology

Background:

Neurofibromatosis type 1 (NF1) is a genetic disorder caused by NF1 tumor suppressor gene mutations.
Plexiform neurofibromas are debilitating tumors in NF1 patients, characterized by complex tumor microenvironments.
Hematopoietic-stromal interactions are critical in tumor initiation, progression, and transformation.

Purpose of the Study:

To investigate the role of cellular and genetic interactions in the tumor microenvironment of plexiform neurofibromas.
To elucidate the feed-forward loop involving Schwann cells, mast cells, and fibroblasts in tumor expansion.
To identify novel therapeutic targets for NF1-associated plexiform neurofibromas.

Main Methods:

Analysis of plexiform neurofibroma microenvironment composition.
Investigation of cellular interactions, including stem cell factor and c-kit signaling.
Utilizing bone marrow transplantation experiments in mouse models with Nf1 haploinsufficiency.

Main Results:

Tumorigenic Schwann cells recruit c-kit expressing mast cells via stem cell factor.
Activated mast cells release inflammatory mediators, stimulating tumor cells, fibroblasts, and blood vessels.
Nf1 haploinsufficiency in the hematopoietic compartment is essential for plexiform neurofibroma tumorigenesis.

Conclusions:

The stem cell factor/c-kit axis plays a crucial role in plexiform neurofibroma development.
Targeted inhibition of the stem cell factor/c-kit pathway represents a viable therapeutic approach.
Understanding tumor-stromal interactions is key to developing effective treatments for NF1.