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The Role of Vascular Cell Adhesion Molecule-1 in Tumor Immune Evasion

Departments of Pathology, Oncology, Obstetrics and Gynecology, and Molecular Microbiology and Immunology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

Requests for reprints: T-C. Wu, Department of Pathology, Johns Hopkins Hospital, CRB II Room 309, 1550 Orleans Street, Baltimore, MD 21231. Phone: 410-614-3899; Fax: 443-287-4295; E-mail: wutc{at}jhmi.edu.

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. [Cancer Res 2007;67(13):6003–6]

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