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[Endoglin as a target of antitumor therapy]
Magdalena Jarosz1, Stanisław Szala
1Centrum Badań Translacyjnych i Biologii Molekularnej Nowotworów, Centrum Onkologii-Instytut im. Marii Skłodowskiej-Curie, Oddział w Gliwicach. mjarosz@io.gliwice.pl
Abstract:
Blood vascular supply significantly affects progression of tumor growth. Inhibition of endothelial cell proliferation by antiangiogenic drugs should lead to growth arrest of both primary tumors and metastases. During the course of lengthy therapy, endothelial cells may, however, become refractory to the action of antiangiogenic agents. Novel approaches to anticancer treatment should explore the issue of drug resistance shown by endothelial cells. One possible therapeutic solution might be tumor immunotherapy directed against antigens expressed on the surface of endothelial cells which co-form tumor blood vasculature. Such therapy is supposed to break immune tolerance to own antigens and to eliminate tumor blood vessel endothelial cells by activating cytotoxic T lymphocytes. This kind of response can be obtained against endoglin (CD105). Endoglin is overexpressed in proliferating endothelial cells which line tumor blood vessels. Presence of endoglin in solid tumor blood vessels has prognostic value in cancer treatment. CD105 is also expressed by certain cancer cells (prostate, melanoma and Ewing sarcoma). It appears that therapeutic strategies directed against endoglin allow several mechanisms of resistance to antiangiogenic drugs to be omitted. The therapeutic approach that we propose, i.e. a tumor blood vessel-destroying strategy combined with immunotherapy, may become an effective therapeutic tool.
Insights
Novel cancer therapies can overcome antiangiogenic drug resistance by targeting tumor blood vessels. Immunotherapy against endoglin (CD105) on endothelial cells offers a promising approach to eliminate tumor vasculature and halt cancer growth.
Area of Science:
- Oncology
- Immunology
- Vascular Biology
Background:
- Tumor growth is highly dependent on blood supply, making antiangiogenic drugs a key treatment strategy.
- Endothelial cells in tumors can develop resistance to antiangiogenic agents during prolonged therapy.
- Drug resistance in tumor endothelial cells necessitates novel therapeutic approaches.
Purpose of the Study:
- To explore novel anticancer treatments addressing drug resistance in tumor endothelial cells.
- To investigate the potential of tumor immunotherapy targeting endothelial cell surface antigens.
- To evaluate endoglin (CD105) as a therapeutic target for breaking immune tolerance and eliminating tumor vasculature.
Main Methods:
- Investigating the role of endothelial cell proliferation in tumor progression.
- Exploring immunotherapy strategies against tumor-associated endothelial cell antigens.
- Assessing the efficacy of targeting endoglin (CD105) for cancer treatment.
Main Results:
- Endoglin (CD105) is overexpressed on proliferating endothelial cells in tumor blood vessels, with prognostic value.
- CD105 is also expressed on certain cancer cells, including prostate, melanoma, and Ewing sarcoma.
- Targeting endoglin may bypass several resistance mechanisms to antiangiogenic drugs.
Conclusions:
- Immunotherapy directed against endoglin (CD105) can activate cytotoxic T lymphocytes to eliminate tumor blood vessel endothelial cells.
- A combined strategy of tumor blood vessel destruction and immunotherapy holds potential as an effective therapeutic tool.
- Targeting endoglin presents a viable strategy to overcome resistance to antiangiogenic therapies.
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