rdf:type |
|
lifeskim:mentions |
umls-concept:C0001483,
umls-concept:C0007634,
umls-concept:C0012655,
umls-concept:C0017262,
umls-concept:C0024348,
umls-concept:C0029016,
umls-concept:C0040682,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0205410,
umls-concept:C0333348,
umls-concept:C1167395,
umls-concept:C1709313,
umls-concept:C2911684
|
pubmed:issue |
18
|
pubmed:dateCreated |
1986-10-22
|
pubmed:abstractText |
Mammalian cells transformed by nononcogenic human adenoviruses exhibit high susceptibility to destruction by host mononuclear inflammatory cells. We have analyzed the viral gene regulation of the susceptibility of transformed cells to lysis by natural killer cells and activated macrophages. Comparisons of target cell lines transformed by overlapping segments of the adenovirus E1-transforming gene region revealed that isolated expression of a single oncogene, E1A, was sufficient to cause increased cytolytic susceptibility in the absence of detectable transformed cell-surface expression of viral transplantation antigens and irrespective of histocompatibility antigen identity between killer cells and target cells. These results suggest that oncogene functions that are not linked to the expression of previously recognized cell-surface target structures may actively induce neoplastic cell elimination by components of the host immune surveillance system.
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pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-14468462,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-2946932,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-3018533,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-3022137,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-310123,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-3843807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-3878030,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-3973965,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-3989909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-404387,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-4215075,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-427789,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-4612107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-4706286,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-494494,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6191867,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6197809,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6239909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6242485,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6262659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6298123,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6310610,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6319497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6334304,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6353747,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6605479,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6690708,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6705049,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6710160,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-6854738,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-7025208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-7039092,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-7097863,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-7147716,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-7356685,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2944117-886304
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0027-8424
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
83
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
6965-9
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:2944117-Adenovirus Early Proteins,
pubmed-meshheading:2944117-Adenoviruses, Human,
pubmed-meshheading:2944117-Cell Line,
pubmed-meshheading:2944117-Cell Transformation, Neoplastic,
pubmed-meshheading:2944117-Cell Transformation, Viral,
pubmed-meshheading:2944117-Cytotoxicity, Immunologic,
pubmed-meshheading:2944117-Genes, Viral,
pubmed-meshheading:2944117-Killer Cells, Natural,
pubmed-meshheading:2944117-Macrophages,
pubmed-meshheading:2944117-Oncogene Proteins, Viral,
pubmed-meshheading:2944117-Oncogenes,
pubmed-meshheading:2944117-Phenotype,
pubmed-meshheading:2944117-RNA, Messenger
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pubmed:year |
1986
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pubmed:articleTitle |
Expression of the adenovirus E1A oncogene during cell transformation is sufficient to induce susceptibility to lysis by host inflammatory cells.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|