Abstract
Dendritic cells (DC) play a crucial role in initiating immune responses to tumors. DC can efficiently present antigens from apoptotic tumor cells, but apoptotic cells are thought to lack the inflammatory signals required to induce DC maturation. Here, we show that apoptosis of 67NR mouse carcinoma cells via the Fas (CD95) pathway or induced by the anticancer drug bortezomib (PS-341) but not by ultraviolet irradiation is associated with the production of maturation signals for DC. These data have important implications for the effects of chemotherapy on antitumor immunity in solid and hematologic malignancies.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Apoptosis / drug effects
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Apoptosis / physiology*
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Apoptosis / radiation effects
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Boronic Acids / pharmacology
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Bortezomib
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Cell Line, Tumor
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Dendritic Cells / cytology
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Dendritic Cells / immunology*
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Mammary Neoplasms, Experimental / drug therapy
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Mammary Neoplasms, Experimental / immunology*
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Mammary Neoplasms, Experimental / pathology
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Mice
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Mice, Inbred BALB C
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Pyrazines / pharmacology
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Signal Transduction / radiation effects
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Tamoxifen / analogs & derivatives*
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Tamoxifen / pharmacology
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fas Receptor / metabolism
Substances
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Antineoplastic Agents
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Boronic Acids
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Pyrazines
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fas Receptor
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Tamoxifen
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afimoxifene
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Bortezomib