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Updated: Nov 10, 2025

Isolation and Culture Expansion of Tumor-specific Endothelial Cells
Published on: October 14, 2015
Hot and Cold Tumors: Is Endoglin (CD105) a Potential Target for Vessel Normalization?
Claudia Ollauri-Ibáñez1, Blanca Ayuso-Íñigo1, Miguel Pericacho1
1Renal and Cardiovascular Research Unit, Group of Physiopathology of the Vascular Endothelium (ENDOVAS), Biomedical Research Institute of Salamanca (IBSAL), Department of Physiology and Pharmacology, University of Salamanca, 37007 Salamanca, Spain.
Tumor microenvironment (TME) characteristics determine immunotherapy response. Targeting endoglin (CD105) via vascular normalization may convert cold tumors to hot tumors, improving treatment outcomes.
Area of Science:
- Oncology
- Immunology
- Biomedical Engineering
Background:
- The tumor microenvironment (TME) comprises malignant and normal cells, influencing cancer prognosis and treatment response, particularly immunotherapy.
- Tumors are classified as 'hot' (immunosupportive TME, good immunotherapy response) or 'cold' (immunosuppressive TME, poor immunotherapy response).
- Vascular normalization is a strategy to convert cold tumors into hot tumors, enhancing immunotherapy efficacy.
Purpose of the Study:
- To propose endoglin (CD105) as a therapeutic target for vascular normalization in converting cold tumors to hot tumors.
- To investigate the role of endoglin (CD105) in the key processes of TME generation: angiogenesis, inflammation, and cancer-associated fibroblast (CAF) accumulation.
- To explore the potential of endoglin (CD105) expression analysis for predicting patient response to immunotherapy.
Main Methods:
- Review of existing literature on tumor microenvironment, immunotherapy, vascular normalization, and endoglin (CD105).
- Analysis of endoglin's (CD105) involvement in angiogenesis, inflammation, and cancer-associated fibroblast (CAF) accumulation.
- Examination of current clinical applications of endoglin (CD105) expression analysis in tumor microvascular density assessment.
Main Results:
- Endoglin (CD105) is implicated in angiogenesis, inflammation, and cancer-associated fibroblast (CAF) accumulation, key components of the TME.
- Endoglin (CD105) expression analysis is currently used clinically to assess microvascular density and is linked to poorer prognoses.
- Endoglin (CD105) presents a potential target for vascular normalization strategies aimed at modulating the TME.
Conclusions:
- Endoglin (CD105) is a promising target for vascular normalization to transform immunosuppressive TMEs into immunosupportive ones.
- Assessing endoglin (CD105) expression in tumors could serve as a predictive biomarker for immunotherapy response.
- Targeting endoglin (CD105) offers a potential therapeutic avenue to improve outcomes for patients with cold tumors.
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