Linked Life Data

20197645

Source:http://linkedlifedata.com/resource/pubmed/id/20197645

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-5-27
pubmed:abstractText
Ataxia telangiectasia (AT) cells, with their defective double-strand break (DSB) repair processes, exhibit high sensitivity to low-LET radiation such as X-rays irradiation and gamma beams. Since heavy ion beam treatment for cancer is becoming increasingly common in Japan and elsewhere, it is important to also determine their sensitivity to high-LET radiation. For this purpose we irradiated AT and normal human cells immortalized with the human telomerase gene using high- (24-60 keV/microm carbon and 200 keV/microm iron ions) or low-LET (X-rays) radiation in non-proliferative conditions. In normal cells the RBE (relative biological effectiveness) of carbon and iron ions increased from 1.19 to 1.81 in proportion to LET. In contrast, their RBE in AT cells increased from 1.32 at 24 keV/microm to 1.59 at 40 keV/microm, and exhibited a plateau at over 40 keV/microm. In normal cells most gamma-H2AX foci induced by both carbon- and iron-ion beams had disappeared at 40 h. In AT cells, however, a significant number of gamma-H2AX foci were still observed at 40 h. The RBEs found in the AT cells after heavy-ion irradiation were consistent with the effects predicted from the presence of non-homologous end joining defects. The DSBs remaining after heavy-ion irradiation suggested defects in the AT cells' DSB repair ability.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0449-3060
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
251-5
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
AT cells show dissimilar hypersensitivity to heavy-ion and X-rays irradiation.
pubmed:affiliation
Central Laboratory and Radiation Biology, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan .
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't