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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2006-7-17
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pubmed:abstractText |
The tumor suppressor STAT1 is considered a key regulator of the surveillance of developing tumors. Here, we describe an unexpected tumor-promoting role for STAT1 in leukemia. STAT1(-/-) mice are partially protected from leukemia development, and STAT1(-/-) tumor cells induce leukemia in RAG2(-/-) and immunocompetent mice with increased latency. The low MHC class I protein levels of STAT1(-/-) tumor cells enable efficient NK cell lysis and account for the enhanced tumor clearance. Strikingly, STAT1(-/-) tumor cells acquire increased MHC class I expression upon leukemia progression. These findings define STAT1 as a tumor promoter in leukemia development. Furthermore, we describe the upregulation of MHC class I expression as a general mechanism that allows for the escape of hematopoietic malignancies from immune surveillance.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins, Fusion,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins v-abl,
http://linkedlifedata.com/resource/pubmed/chemical/Rag2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/TEL-JAK2 fusion protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1535-6108
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
77-87
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16843267-Animals,
pubmed-meshheading:16843267-B-Lymphocytes,
pubmed-meshheading:16843267-Cell Line, Tumor,
pubmed-meshheading:16843267-Cell Proliferation,
pubmed-meshheading:16843267-Cell Survival,
pubmed-meshheading:16843267-Cell Transformation, Neoplastic,
pubmed-meshheading:16843267-DNA-Binding Proteins,
pubmed-meshheading:16843267-Disease Progression,
pubmed-meshheading:16843267-Genotype,
pubmed-meshheading:16843267-Histocompatibility Antigens Class I,
pubmed-meshheading:16843267-Interferon-gamma,
pubmed-meshheading:16843267-Killer Cells, Natural,
pubmed-meshheading:16843267-Leukemia, Experimental,
pubmed-meshheading:16843267-Mice,
pubmed-meshheading:16843267-Mice, Inbred BALB C,
pubmed-meshheading:16843267-Mice, Inbred C57BL,
pubmed-meshheading:16843267-Mice, Knockout,
pubmed-meshheading:16843267-Oncogene Proteins, Fusion,
pubmed-meshheading:16843267-Oncogene Proteins v-abl,
pubmed-meshheading:16843267-Phenotype,
pubmed-meshheading:16843267-STAT1 Transcription Factor,
pubmed-meshheading:16843267-Stem Cells,
pubmed-meshheading:16843267-Survival Analysis
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pubmed:year |
2006
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pubmed:articleTitle |
STAT1 acts as a tumor promoter for leukemia development.
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pubmed:affiliation |
Department of Pharmacology, Medical University of Vienna (MUW), Vienna A-1090, Austria.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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