Related Experiment Video
Updated: Jul 5, 2026
12:16
Patient Derived Cell Culture and Isolation of CD133+ Putative Cancer Stem Cells from Melanoma
Published on: March 13, 2013
Cutaneous cancer stem cells: beta-catenin strikes again
1Centre for Cutaneous Research, Barts and The London School of Medicine and Dentistry, Institute of Cell and Molecular Science, 4 Newark Street, London E1 2AT, UK. k.braun@qmul.ac.uk
Cell Stem Cell
|May 9, 2008
Summary
Cancer stem cells (CSCs) are tumor cells that can self-renew. Researchers found that CD34(+) cells in skin tumors need beta-catenin signaling to maintain their cancer stem cell properties.
Area of Science:
- Oncology
- Stem Cell Biology
- Dermatology
Background:
- Cancer stem cells (CSCs) are a critical component of tumor development and progression.
- CSCs possess self-renewal capabilities, similar to normal tissue stem cells.
- Identifying CSC markers and regulatory pathways is crucial for targeted cancer therapies.
Purpose of the Study:
- To identify specific cell populations within epidermal tumors exhibiting cancer stem cell characteristics.
- To investigate the signaling pathways essential for maintaining the CSC phenotype in these cells.
Main Methods:
- Utilized flow cytometry to identify and isolate CD34(+) cells from epidermal tumors.
- Analyzed the role of beta-catenin signaling in the self-renewal and maintenance of the CSC phenotype.
Main Results:
- A distinct population of CD34(+) cells was identified in epidermal tumors.
- These CD34(+) cells demonstrated properties consistent with cancer stem cells.
- Beta-catenin signaling was found to be indispensable for sustaining the CSC phenotype in these identified cells.
Conclusions:
- CD34(+) cells represent a key cancer stem cell subpopulation in epidermal tumors.
- Targeting beta-catenin signaling could be a potential therapeutic strategy for eliminating CSCs in skin cancers.
Related Concept Videos
02:40Cancer Stem Cells and Tumor Maintenance
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.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
02:40Cancer Stem Cells and Tumor Maintenance
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.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
01:18Distinctive Features of Adult Stem Cells vs Cancer Stem Cells
A stem cell is an unspecialized cell that can divide without limit as needed and can, under specific conditions, differentiate into specialized cells.
Adult stem cells
Adult stem cells are tissue-specific; hence, they divide to develop the tissue from which they originate. One type of adult stem cell is the epithelial stem cell, which gives rise to the keratinocytes in the multiple layers of epithelial cells in the epidermis of the skin. Adult bone marrow has three distinct types of stem cells:...
Adult stem cells
Adult stem cells are tissue-specific; hence, they divide to develop the tissue from which they originate. One type of adult stem cell is the epithelial stem cell, which gives rise to the keratinocytes in the multiple layers of epithelial cells in the epidermis of the skin. Adult bone marrow has three distinct types of stem cells:...
01:12Renewal of Skin Epidermal Stem Cells
The skin is divided into epidermis, dermis, and hypodermis, the skin's outermost, middle, and inner layers. The human epidermal layer regularly undergoes renewal, where old, dead cells are replaced by new cells. Epidermal stem cells or EpiSCs divide and differentiate to restore the lost cells. For the renewal process, some EpiSCs continuously self-renew. In contrast, few others differentiate into transit-amplifying cells, which later form prickle or spinous cells, followed by granular cells,...
01:23Catenins
Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
Catenins in Cell Junctions
Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the adherens...
Catenins in Cell Junctions
Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the adherens...
02:30Metastasis
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...
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...