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Published on: September 27, 2013
Targeting cancer stem cells to modulate alternative vascularization mechanisms
Elena Monzani1, Caterina Am La Porta
1Molecular Oncology Laboratory, Department of Biomolecular Science and Biotechnology, University of Milan, 20133, Milan, Italy.
Tumor vascularization involves various mechanisms, including vasculogenic mimicry. This study critically compares vasculogenic mimicry with cancer stem cells and bone marrow stem cells, proposing models for alternative vascular patterns.
Area of Science:
- Oncology
- Cell Biology
- Biomedical Engineering
Background:
- Tumor vascularization is crucial for cancer growth and metastasis.
- Mechanisms include angiogenesis, co-option, mosaic vessels, and vasculogenic mimicry.
- Vasculogenic mimicry involves tumor cells forming vessel-like structures, distinct from endothelial-lined vessels.
Purpose of the Study:
- To critically compare vasculogenic mimicry with cancer stem cells (CSCs) and bone marrow-derived stem cells (BMSCs).
- To explore the potential role of stem cell populations in alternative vascularization patterns.
- To discuss existing literature and propose models for tumor vascularization.
Main Methods:
- Literature review and critical analysis of existing data.
- Comparison of vasculogenic mimicry, CSCs, and BMSCs.
- Development of theoretical models for alternative vascularization.
Main Results:
- Vasculogenic mimicry differs from mosaic vessels, with tumor cells lacking endothelial markers.
- Vasculogenic mimicry has been observed in multiple myeloma, potentially involving bone marrow macrophages.
- Stem cell populations (CSCs and BMSCs) may drive alternative vascularization patterns.
Conclusions:
- Alternative vascularization patterns in tumors may be attributed to the presence of CSCs or BMSCs.
- Further research is needed to elucidate the precise mechanisms and therapeutic implications.
- Potential pharmacological strategies targeting these pathways will be discussed.
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