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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5186
|
pubmed:dateCreated |
1994-12-7
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pubmed:abstractText |
The therapeutic responsiveness of genetically defined tumors expressing or devoid of the p53 tumor suppressor gene was compared in immunocompromised mice. Tumors expressing the p53 gene contained a high proportion of apoptotic cells and typically regressed after treatment with gamma radiation or adriamycin. In contrast, p53-deficient tumors treated with the same regimens continued to enlarge and contained few apoptotic cells. Acquired mutations in p53 were associated with both treatment resistance and relapse in p53-expressing tumors. These results establish that defects in apoptosis, here caused by the inactivation of p53, can produce treatment-resistant tumors and suggest that p53 status may be an important determinant of tumor response to therapy.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
0036-8075
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
4
|
pubmed:volume |
266
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pubmed:geneSymbol |
p53
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
807-10
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7973635-Animals,
pubmed-meshheading:7973635-Apoptosis,
pubmed-meshheading:7973635-Doxorubicin,
pubmed-meshheading:7973635-Drug Resistance,
pubmed-meshheading:7973635-Fibrosarcoma,
pubmed-meshheading:7973635-Gamma Rays,
pubmed-meshheading:7973635-Genes, p53,
pubmed-meshheading:7973635-Immunocompromised Host,
pubmed-meshheading:7973635-Mice,
pubmed-meshheading:7973635-Mice, Nude,
pubmed-meshheading:7973635-Mutation,
pubmed-meshheading:7973635-Neoplasm Recurrence, Local,
pubmed-meshheading:7973635-Neoplasm Transplantation,
pubmed-meshheading:7973635-Radiation Tolerance
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pubmed:year |
1994
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pubmed:articleTitle |
p53 status and the efficacy of cancer therapy in vivo.
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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
|