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rdf:type |
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lifeskim:mentions |
umls-concept:C0003320,
umls-concept:C0006826,
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0021745,
umls-concept:C0185117,
umls-concept:C0205217,
umls-concept:C0205263,
umls-concept:C0234227,
umls-concept:C0333117,
umls-concept:C0449258,
umls-concept:C0580822,
umls-concept:C1547300,
umls-concept:C1548760,
umls-concept:C1550594,
umls-concept:C2911684
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pubmed:dateCreated |
2011-6-30
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pubmed:abstractText |
Many cancers escape host immunity without losing tumor-specific rejection antigens or MHC class I expression. This study tracks the evolution of one such cancer that developed in a mouse following exposure to ultraviolet light. The primary autochthonous tumor was not highly malignant and was rejected when transplanted into naïve immunocompetent mice. Neoplastic cells isolated from the primary tumor were susceptible to the growth-inhibitory effects of IFN? in vitro, but expressed very low levels of MHC I antigen and were resistant to tumor-specific T cells unless they were first exposed to IFN?. Serial passage of the primary tumor cells in vivo led to a highly aggressive variant that caused fast-growing tumors in normal mice. In vitro, the variant tumor cells showed increased resistance to the growth-inhibitory effects of IFN? but expressed high levels of immunoproteasomes and MHC I molecules and were susceptible to tumor-specific T cells even without prior exposure to IFN?.
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pubmed:grant |
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pubmed:commentsCorrections |
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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:issn |
1424-9634
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pubmed:author |
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