Abstract
Malignant melanoma accounts for most of the increasing mortality from skin cancer. Melanoma cells were found to express Fas (also called Apo-1 or CD95) ligand (FasL). In metastatic lesions, Fas-expressing T cell infiltrates were proximal to FasL+ tumor cells. In vitro, apoptosis of Fas-sensitive target cells occurred upon incubation with melanoma tumor cells; and in vivo, injection of FasL+ mouse melanoma cells in mice led to rapid tumor formation. In contrast, tumorigenesis was delayed in Fas-deficient lpr mutant mice in which immune effector cells cannot be killed by FasL. Thus, FasL may contribute to the immune privilege of tumors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis*
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Fas Ligand Protein
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Humans
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Ligands
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Lymphocytes, Tumor-Infiltrating / cytology
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Lymphocytes, Tumor-Infiltrating / immunology
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Melanoma / immunology*
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Melanoma / metabolism
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Melanoma / pathology
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Melanoma / secondary
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Membrane Glycoproteins / analysis
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Membrane Glycoproteins / biosynthesis
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Membrane Glycoproteins / physiology*
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Mice
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Mice, Inbred C57BL
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T-Lymphocytes, Cytotoxic / cytology*
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T-Lymphocytes, Cytotoxic / immunology
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Tumor Cells, Cultured
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Tumor Escape*
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fas Receptor / biosynthesis
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fas Receptor / physiology*
Substances
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FASLG protein, human
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Fas Ligand Protein
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Fasl protein, mouse
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Ligands
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Membrane Glycoproteins
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fas Receptor