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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2009-1-16
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pubmed:abstractText |
Immune escape describes a critical event whereby tumor cells adopt an immunoresistant phenotype to escape adaptive surveillance. We show that expression of a pivotal negative regulator of T-cell function, B7-H1, correlates with PI(3) kinase activation in breast and prostate cancer patients. B7-H1-mediated immunoresistance can be attenuated by inhibitors of the PI(3) kinase pathway, and is dependent on S6K1-mediated translational regulation of B7-H1 protein. Breast and prostate carcinoma cells with activated PI(3) kinase lose the immunoresistant phenotype after treatment with B7-H1 siRNA. Conversely, breast and prostate carcinoma cells with minimal PI(3) kinase activation adopt an immunoresistant phenotype when engineered to overexpress B7-H1 protein. These observations describe a mechanism for immune escape from tumor dormancy in humans that relates to oncogenesis.
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD274,
http://linkedlifedata.com/resource/pubmed/chemical/CD274 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/PTEN Phosphohydrolase,
http://linkedlifedata.com/resource/pubmed/chemical/PTEN protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ribosomal Protein S6 Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1476-5594
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
28
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
306-12
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:18850006-Adenocarcinoma,
pubmed-meshheading:18850006-Antigens, CD,
pubmed-meshheading:18850006-Antigens, CD274,
pubmed-meshheading:18850006-Breast Neoplasms,
pubmed-meshheading:18850006-Cell Line, Tumor,
pubmed-meshheading:18850006-Female,
pubmed-meshheading:18850006-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:18850006-Gene Knockdown Techniques,
pubmed-meshheading:18850006-Humans,
pubmed-meshheading:18850006-Male,
pubmed-meshheading:18850006-Neoplasm Proteins,
pubmed-meshheading:18850006-PTEN Phosphohydrolase,
pubmed-meshheading:18850006-Phenotype,
pubmed-meshheading:18850006-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:18850006-Prostatic Neoplasms,
pubmed-meshheading:18850006-Protein Kinase Inhibitors,
pubmed-meshheading:18850006-RNA, Small Interfering,
pubmed-meshheading:18850006-Recombinant Fusion Proteins,
pubmed-meshheading:18850006-Ribosomal Protein S6 Kinases,
pubmed-meshheading:18850006-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:18850006-Tumor Escape
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pubmed:year |
2009
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pubmed:articleTitle |
PI(3) kinase is associated with a mechanism of immunoresistance in breast and prostate cancer.
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pubmed:affiliation |
Department of Neurological Surgery, University of California San Francisco, San Francisco, CA 94143, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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