rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
1994-4-21
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pubmed:abstractText |
p53-deficient mouse embryonic fibroblasts were used to establish a direct mechanism of tumor suppression by p53 involving the destruction of oncogene-expressing cells by apoptosis. The absence of p53 enhanced cell growth, appeared sufficient for immortalization, and allowed a single oncogene [adenovirus early region 1A (E1A)] to transform cells to a tumorigenic state. p53 suppressed transformation of E1A-expressing cells by apoptosis. Apoptosis was associated with p53 stabilization and was triggered by environmental signals that normally suppress cell growth. Absence of even a single p53 allele significantly enhanced cell growth and survival. Although abrogation of apoptosis allowed transformation by E1A alone, escape from apoptosis susceptibility was not a prerequisite for tumor growth. Consequently, p53 mutation could enhance the survival of malignant cells expressing oncogenes activated early in tumor progression.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1356076,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1406975,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1406976,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1423616,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1457005,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1505019,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1533443,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1555236,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1570319,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1614522,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1752433,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1851867,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1852210,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1933891,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-1996096,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-2188735,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-2223387,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/8134344-8479523
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
|
pubmed:volume |
91
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
2026-30
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8134344-Adenovirus E1A Proteins,
pubmed-meshheading:8134344-Animals,
pubmed-meshheading:8134344-Apoptosis,
pubmed-meshheading:8134344-Cell Division,
pubmed-meshheading:8134344-Cell Line,
pubmed-meshheading:8134344-Cell Transformation, Neoplastic,
pubmed-meshheading:8134344-Fibroblasts,
pubmed-meshheading:8134344-Male,
pubmed-meshheading:8134344-Mice,
pubmed-meshheading:8134344-Mice, Nude,
pubmed-meshheading:8134344-Oncogenes,
pubmed-meshheading:8134344-Tumor Suppressor Protein p53
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pubmed:year |
1994
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pubmed:articleTitle |
Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells.
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pubmed:affiliation |
Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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