| pubmed-article:8134344 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8134344 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8134344 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:8134344 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
| pubmed-article:8134344 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:8134344 | pubmed:dateCreated | 1994-4-21 | lld:pubmed |
| pubmed-article:8134344 | 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. | lld:pubmed |
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| pubmed-article:8134344 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8134344 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8134344 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8134344 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:8134344 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8134344 | pubmed:author | pubmed-author:HousmanD EDE | lld:pubmed |
| pubmed-article:8134344 | pubmed:author | pubmed-author:RuleyH EHE | lld:pubmed |
| pubmed-article:8134344 | pubmed:author | pubmed-author:JacksTT | lld:pubmed |
| pubmed-article:8134344 | pubmed:author | pubmed-author:LoweS WSW | lld:pubmed |
| pubmed-article:8134344 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8134344 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:8134344 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:8134344 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8134344 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8134344 | pubmed:pagination | 2026-30 | lld:pubmed |
| pubmed-article:8134344 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8134344 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8134344 | pubmed:articleTitle | Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells. | lld:pubmed |
| pubmed-article:8134344 | pubmed:affiliation | Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139. | lld:pubmed |
| pubmed-article:8134344 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8134344 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8134344 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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