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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...
Tumor Immunotherapy01:27

Tumor Immunotherapy

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.
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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Related Experiment Video

Updated: May 8, 2026

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

Tumor and its microenvironment: a synergistic interplay.

Veronica Catalano1, Alice Turdo, Simone Di Franco

  • 1University of Palermo, Department of Surgical and Oncological Sciences, Laboratory of Cellular and Molecular Pathophysiology, Via Liborio Giuffrè, 5, 90127 Palermo, Italy.

Seminars in Cancer Biology
|September 10, 2013
PubMed
Summary

The tumor microenvironment and cancer stem cells (CSCs) drive metastasis. Targeting stromal interactions and factors like hypoxia-inducible factors (HIFs) and vascular endothelial growth factors (VEGFs) is key to preventing cancer spread.

Keywords:
AngiogenesisCAFsCAMsCRCCSCsECMEMTGSHHIFHypoxiaMMPsROSTumor microenvironmentVEGFcancer stem cellscancer-associated fibroblastscancer-associated macrophagescolorectal cancerepithelial mesenchymal transitionextracellular matrixhypoxia-inducible factormatrix metalloproteinasereactive oxygen speciesreduced glutathionevascular endothelial growth factor

More Related Videos

Microfluidic Device for Recreating a Tumor Microenvironment in Vitro
16:18

Microfluidic Device for Recreating a Tumor Microenvironment in Vitro

Published on: November 20, 2011

Related Experiment Videos

Last Updated: May 8, 2026

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

Microfluidic Device for Recreating a Tumor Microenvironment in Vitro
16:18

Microfluidic Device for Recreating a Tumor Microenvironment in Vitro

Published on: November 20, 2011

Area of Science:

  • Oncology
  • Cancer Biology
  • Tumor Microenvironment Research

Background:

  • The tumor microenvironment (TME) is a complex network influencing tumor progression and metastasis.
  • Cancer stem cells (CSCs) are critical for tumor maintenance and metastatic colonization.
  • CSCs possess antioxidant systems, like glutathione (GSH)-dependent pathways, to combat oxidative stress (ROS).

Purpose of the Study:

  • To review the synergistic roles of hypoxia-inducible factors (HIFs) and vascular endothelial growth factors (VEGFs) in promoting metastasis.
  • To integrate emerging models of tumor progression and metastatic outgrowth.
  • To highlight the importance of targeting stromal interactions for improved cancer therapeutics.

Main Methods:

  • Literature review and synthesis of current research on TME, CSCs, HIFs, and VEGFs.
  • Analysis of mechanisms driving extracellular matrix remodeling, cell activation, and epithelial-mesenchymal transition (EMT).
  • Integration of theories on angiogenesis, tumor cell dissemination, and pre-metastatic niche formation.

Main Results:

  • The TME, including stromal cells and extracellular matrix, actively supports tumor growth and metastasis.
  • CSCs utilize antioxidant defenses to survive stress and promote malignancy.
  • Tumor vasculature, promoted by HIFs and VEGFs, facilitates cancer cell spread and niche formation.

Conclusions:

  • Targeting stromal components and pathways like HIFs and VEGFs offers therapeutic potential against metastasis.
  • Understanding the interplay between CSCs and their microenvironment is crucial for developing effective cancer treatments.
  • The review integrates key factors contributing to metastatic outgrowth, providing a comprehensive overview for researchers.