期刊
CANCER RESEARCH
卷 67, 期 13, 页码 6003-6006出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-07-1543
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资金
- NCI NIH HHS [R01 CA114425-01, P50 CA098252, P50 CA098252-02, U19 CA113341-01, U19 CA113341, R01 CA114425, 1P50 CA098252-02, 1R01 CA114425-01] Funding Source: Medline
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.
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