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On the other hand, tumor-associated vascular endothelial cells can express programmed death-ligand 1 (PD-L1) and Fas ligand (FasL), selectively inhibit cytotoxic T cells (CTLs), and promote regulatory T cell (Treg) function to enhance the immunosuppressive TME. On the one hand, restricted tumor vascular perfusion blocks the transfer of chemotherapeutic and immunotherapeutic agents to the tumor interior and eliminates infiltrated immunosuppressive cells in the TME. Tumor vasculature is unevenly distributed and chaotic.
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We also discussed biomarkers to monitor the response to antiangiogenic agents plus immunotherapy and the challenges in this emerging field.Įnhanced angiogenesis is the hallmark of cancer. In this article, we reviewed the crosstalk between the breast cancer vascular system and the immune microenvironment, discussed the mechanisms by which antiangiogenic therapy reverses the immunosuppressive TME and emphasized the clinical evidence of antiangiogenic therapy plus immunotherapy. Targeting angiogenesis represent a potential option to reverse tumor-associated perfusion abnormalities and the immunosuppressive microenvironment. Given this evidence, tumor angiogenesis could interact with the immune TME. In preclinical research, antiangiogenic therapy has been shown to reverse abnormal tumor blood perfusion, promote immune cell infiltration and normalize the immune TME. Antiangiogenic therapy has been widely studied for a long time, and most antiangiogenic agents target vascular endothelial growth factors (VEGFs) and VEGF receptors (VEGFRs). Although ICB could reactivate dysfunctional or depleted T cells, these reactivated T cells could not infiltrate into the center of solid tumors to exert antitumor effects.
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Hence, there is a need to explore how to intensify treatment based on immunotherapy to achieve more survival benefits. However, only 10–30% of breast cancer patients benefit from ICB immunotherapy.
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Revolutionary changes in cancer treatment have occurred with the continuous development of immune checkpoint blockade (ICB) immunotherapy. The abnormal structure of the tumor vasculature and restricted blood perfusion prevent immune cells from infiltrating tumors efficiently, which results in an unbalanced and immunosuppressive tumor microenvironment (TME). Angiogenesis, which refers to the formation of abnormally immature vessels, often accompanies tumorigenesis. The signal imbalance between proangiogenic and antiangiogenic molecules leads to tumor vascular dysfunction. The combination of antiangiogenic therapy and immunotherapy could be a potential therapeutic strategy for treatment of breast cancer to promote tumor vasculature normalization and increase the efficiency of immunotherapy.
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In addition, we summarize the preclinical research and ongoing clinical research related to the combination of antiangiogenic therapy with immunotherapy, discuss the underlying mechanisms, and provide a view for future developments. Combining antiangiogenic therapy with immunotherapy could interrupt abnormal tumor vasculature-immunosuppression crosstalk, increase effector immune cell infiltration, improve immunotherapy effectiveness, and reduce the risk of immune-related adverse events. This article discusses the immunosuppressive characteristics of the breast cancer TME and outlines the interaction between the tumor vasculature and the immune system. Combining antiangiogenic therapy with immunotherapy might represent a promising option for the treatment of breast cancer. Antangiogenic therapy could improve local perfusion, relieve tumor microenvironment (TME) hypoxia, and reverse the immunosuppressive state. Immunotherapy efficacy depends on the accumulation and activity of tumor-infiltrating immune cells (TIICs). Tumor angiogenesis induces local hypoxia and recruits immunosuppressive cells, whereas hypoxia subsequently promotes tumor angiogenesis.