pubmed-article:20305132 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0006142 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0043210 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0015333 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0014507 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0920506 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0851346 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0919524 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C2603343 | lld:lifeskim |
pubmed-article:20305132 | lifeskim:mentions | umls-concept:C0441988 | lld:lifeskim |
pubmed-article:20305132 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:20305132 | pubmed:dateCreated | 2010-4-7 | lld:pubmed |
pubmed-article:20305132 | pubmed:abstractText | Ionizing radiation is a known mutagen and an established breast carcinogen. The ATM gene is a key regulator of cellular responses to the DNA damage induced by ionizing radiation. We investigated whether genetic variants in ATM play a clinically significant role in radiation-induced contralateral breast cancer in women. | lld:pubmed |
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pubmed-article:20305132 | pubmed:language | eng | lld:pubmed |
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pubmed-article:20305132 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20305132 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20305132 | pubmed:month | Apr | lld:pubmed |
pubmed-article:20305132 | pubmed:issn | 1460-2105 | lld:pubmed |
pubmed-article:20305132 | pubmed:author | pubmed-author:MellemkjaerLe... | lld:pubmed |
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pubmed-article:20305132 | pubmed:author | pubmed-author:LynchCharles... | lld:pubmed |
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pubmed-article:20305132 | pubmed:author | pubmed-author:RosensteinBar... | lld:pubmed |
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