The role of vascular cell adhesion molecule-1 in tumor immune evasion.
Tumor immune escape is a critical trait of cancer but the mechanisms involved have yet to fully emerge. One recent study has shown that tumor cells can escape T-cell immunity by overexpressing the endothelial cell adhesion molecule vascular cell adhesion molecule-1 (VCAM-1), which normally mediates leukocyte extravasion to sites of tissue inflammation. Renal cell carcinoma (RCC) was identified as one tumor type where VCAM-1 is commonly highly overexpressed. Together, our findings suggest that RCCs might exploit VCAM-1 overexpression for immune escape.
Wu
T-C
TC
Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA. wutc@jhmi.edu
D002292:Carcinoma, Renal Cell / Q000276:immunology* / Q000473:pathology; D002448:Cell Adhesion; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D007107:Immune System; D016023:Integrins / Q000378:metabolism; D008113:Liver Neoplasms / Q000276:immunology* / Q000473:pathology; D008954:Models, Biological; D009361:Neoplasm Invasiveness; D009369:Neoplasms / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis* / Q000502:physiology*
D016023:Integrins; D019010:Vascular Cell Adhesion Molecule-1