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Endothelial cell-selective adhesion molecule (ESAM) is a transmembrane glycoprotein belonging to the immunoglobulin superfamily, primarily localized at the tight junctions of endothelial cells and on the surface of activated platelets (UniProt Q96AP7). It functions as a homophilic adhesion molecule that regulates vascular permeability and is crucial for the process of angiogenesis, particularly in pathological contexts like tumor growth (PubMed: 11533235). ESAM also facilitates leukocyte extravasation during inflammatory responses by modulating the integrity of the endothelial barrier (PubMed: 15155605). In oncology, ESAM is considered a promising therapeutic target because its inhibition can disrupt the formation of new blood vessels within tumors, thereby limiting nutrient supply and metastatic spread (PubMed: 22492958). Additionally, ESAM serves as a marker for hematopoietic stem cells and is involved in their recovery after bone marrow injury (PubMed: 17431101). While clinical-stage drugs specifically targeting ESAM are currently limited, experimental monoclonal antibodies are being utilized in research to explore its potential in treating cancer and chronic inflammatory diseases.
Inhibition of homophilic ESAM-ESAM interactions to disrupt endothelial cell migration, tube formation, and leukocyte recruitment.
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