Source:http://linkedlifedata.com/resource/pubmed/id/16170360
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2006-1-13
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| pubmed:abstractText |
Knowledge of the type of biological reaction to chemotherapy is a prerequisite for its rational enhancement. We previously showed that irinotecan-induced DNA damage triggers in the HCT116p53(wt) colon carcinoma cell line a long-term cell cycle arrest and in HCT116p53(-/-) cells apoptosis (Magrini et al., 2002). To compare the contribution of long-term cell cycle arrest and that of apoptosis to inhibition of cell proliferation after irinotecan-induced DNA damage, we used this isogenic system as well as the cell lines LS174T (p53(wt)) and HT-29 (p53(mut)). Both p53(wt) cell lines responded to damage by undergoing a long-term tetraploid G1 arrest, whereas the p53(mut) cell lines underwent apoptosis. Cell cycle arrest as well as apoptosis caused a similar delay in cell proliferation. Irinotecan treatment also induced in mouse tumours derived from the p53(wt) cell lines a tetraploid G1 arrest and in those derived from the p53-deficient cell lines a transient G2/M arrest and apoptosis. The delay of tumour growth was in the same range in both groups, that is, arrest- and apoptosis-mediated tumour growth inhibition was comparable. In conclusion, cell cycle arrest as well as apoptosis may be equipotent mechanisms mediating the chemotherapeutic effects of irinotecan.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents, Phytogenic,
http://linkedlifedata.com/resource/pubmed/chemical/Camptothecin,
http://linkedlifedata.com/resource/pubmed/chemical/Topoisomerase I Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53,
http://linkedlifedata.com/resource/pubmed/chemical/irinotecan
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0950-9232
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
12
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| pubmed:volume |
25
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
165-75
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:16170360-Animals,
pubmed-meshheading:16170360-Antineoplastic Agents, Phytogenic,
pubmed-meshheading:16170360-Apoptosis,
pubmed-meshheading:16170360-Blotting, Western,
pubmed-meshheading:16170360-Camptothecin,
pubmed-meshheading:16170360-Cell Cycle,
pubmed-meshheading:16170360-Cell Proliferation,
pubmed-meshheading:16170360-Colonic Neoplasms,
pubmed-meshheading:16170360-DNA Damage,
pubmed-meshheading:16170360-Female,
pubmed-meshheading:16170360-Flow Cytometry,
pubmed-meshheading:16170360-Humans,
pubmed-meshheading:16170360-Mice,
pubmed-meshheading:16170360-Mice, Inbred BALB C,
pubmed-meshheading:16170360-Mice, Nude,
pubmed-meshheading:16170360-Mutation,
pubmed-meshheading:16170360-Necrosis,
pubmed-meshheading:16170360-Ploidies,
pubmed-meshheading:16170360-Topoisomerase I Inhibitors,
pubmed-meshheading:16170360-Tumor Cells, Cultured,
pubmed-meshheading:16170360-Tumor Suppressor Protein p53
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| pubmed:year |
2006
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| pubmed:articleTitle |
Equivalent effect of DNA damage-induced apoptotic cell death or long-term cell cycle arrest on colon carcinoma cell proliferation and tumour growth.
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| pubmed:affiliation |
Department of Gastroenterology, Charité-Universitaetsmedizin Berlin, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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