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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0033414,
umls-concept:C0035015,
umls-concept:C0035820,
umls-concept:C0185117,
umls-concept:C0205359,
umls-concept:C0253023,
umls-concept:C0439662,
umls-concept:C0870509,
umls-concept:C1548437,
umls-concept:C1710493,
umls-concept:C1882923,
umls-concept:C2911684
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pubmed:issue |
4
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pubmed:dateCreated |
2001-3-19
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pubmed:abstractText |
Tumors escape immune-mediated rejection by a variety of mechanisms during tumor progression. The elucidation of these mechanisms in vivo suffers from a lack of suitable models of spontaneous tumor formation escaping active specific immunotherapy (ASI). In a rat neu transgenic (rNeu-TG) mouse model of spontaneous breast tumor formation, we showed that rNeu-TG mice developed late escape tumors despite the presence of a persistent rNeu-specific immune response after ASI. Cell suspensions derived from these escape tumors grew in vaccinated tumor-free mice, whereas injected spontaneous tumor cells were rejected. Escape tumors retained rNeu or MHC class I expression but significantly upregulated Fas (CD95, Apo-1) ligand. We further demonstrated that Fas-L on escape tumor cells correlated with apoptosis of infiltrating T lymphocytes. Thus, our results provide evidence that spontaneous breast tumors upregulate Fas-L expression after vaccination that may promote tumor escape in vivo after ASI.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0020-7136
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2001 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
91
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
529-37
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11251977-3T3 Cells,
pubmed-meshheading:11251977-Animals,
pubmed-meshheading:11251977-Apoptosis,
pubmed-meshheading:11251977-Breast Neoplasms,
pubmed-meshheading:11251977-Cancer Vaccines,
pubmed-meshheading:11251977-Cell Separation,
pubmed-meshheading:11251977-Fas Ligand Protein,
pubmed-meshheading:11251977-Female,
pubmed-meshheading:11251977-Flow Cytometry,
pubmed-meshheading:11251977-Genes, MHC Class I,
pubmed-meshheading:11251977-Immunohistochemistry,
pubmed-meshheading:11251977-Lymphocytes,
pubmed-meshheading:11251977-Mammary Neoplasms, Animal,
pubmed-meshheading:11251977-Membrane Glycoproteins,
pubmed-meshheading:11251977-Mice,
pubmed-meshheading:11251977-Mice, Transgenic,
pubmed-meshheading:11251977-Neoplasm Transplantation,
pubmed-meshheading:11251977-Neoplasms, Experimental,
pubmed-meshheading:11251977-Polymerase Chain Reaction,
pubmed-meshheading:11251977-Rats,
pubmed-meshheading:11251977-Receptor, erbB-2,
pubmed-meshheading:11251977-T-Lymphocytes,
pubmed-meshheading:11251977-Time Factors,
pubmed-meshheading:11251977-Up-Regulation
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pubmed:year |
2001
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pubmed:articleTitle |
Role of Fas ligand expression in promoting escape from immune rejection in a spontaneous tumor model.
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pubmed:affiliation |
Department of Clinical Research, University of Bern, 35 Murtenstrasse, 3010 Bern, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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