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Cancer Stem Cells and Tumor Maintenance

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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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.
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Three-Dimensional Culture of Murine Colonic Crypts to Study Intestinal Stem Cell Function Ex Vivo

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Claudins and cancer stem cells.

Kursad Turksen¹

¹Regenerative Medicine Program, Sprott Centre for Stem Cell Research at the Ottawa Hospital Research Institute, 501 Smyth Road-CCW5226, Ottawa, ON K1Y 8L6, Canada. kturksen@ohri.ca

Stem Cell Reviews and Reports

|April 29, 2011

Summary

Most epithelial tumors are sustained by cancer stem cells (CSCs). The Claudin-low phenotype and epithelial-mesenchymal transition (EMT) are key factors in CSCs, potentially offering new therapeutic targets.

Area of Science:

Oncology
Cell Biology
Cancer Research

Background:

Epithelial tumors are often sustained by cancer stem cells (CSCs) possessing self-renewal and differentiation capabilities.
Recent research highlights the Claudin-low phenotype in CSCs and its connection to the epithelial-mesenchymal transition (EMT).

Purpose of the Study:

To explore the relationship between cancer stem cells (CSCs), the Claudin-low phenotype, and the epithelial-mesenchymal transition (EMT).
To identify potential therapeutic strategies by understanding the 'axis-of-evil' in cancer involving CSCs, EMT, and Claudins.

Main Methods:

Literature review and synthesis of recent findings on CSCs, Claudins, and EMT.
Analysis of the functional implications of the Claudin-low phenotype in CSCs.
Investigation of the role of CSCs, EMT, and Claudins in tumor progression.

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Main Results:

CSCs are crucial for maintaining epithelial tumors.
The Claudin-low phenotype is associated with CSCs and plays a significant role in EMT.
The interplay between CSCs, EMT, and Claudins represents a critical axis in cancer development.

Conclusions:

Understanding the CSCs-EMT-Claudin axis is vital for cancer research.
Targeting this axis holds promise for developing novel cancer therapeutics.