Source:http://linkedlifedata.com/resource/pubmed/id/16563661
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2006-6-6
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pubmed:abstractText |
A line of investigation in the search for sensitizing tumor cells to chemotherapy or radiotherapy relies on the selection of DNA repair inhibitors. In the area of DNA repair mechanisms, DNA-dependent protein kinase (DNA-PK) represents a key complex. Indeed DNA-PK is involved in the non-homologous end joining (NHEJ) process that corresponds to the major activity responsible for cell survival after ionizing radiation or chemotherapeutic treatment producing DNA double strand breaks. DNA-PK belongs to the PI3-K related kinase family and specific inhibitors have been recently selected and evaluated as radio- and chemo-sensitizers. These drugs, along with other ways to inhibit the DSBs repair process, are presented and discussed.
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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 |
May
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pubmed:issn |
0369-8114
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
185-93
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading | |
pubmed:year |
2006
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pubmed:articleTitle |
The DNA repair complex DNA-PK, a pharmacological target in cancer chemotherapy and radiotherapy.
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pubmed:affiliation |
Institut de Pharmacologie et Biologie Structurale (IPBS) UMR CNRS 5089, Toulouse, France. bernard.salles@ipbs.fr
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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