Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-9-27
pubmed:abstractText
Hyperthermia has a radiosensitizing effect, which is one of the most important biological bases for its use in cancer therapy with radiation. Although the mechanism of this effect has not been clarified in molecular terms, possible involvement of either one or both of two major DNA double-strand break (DSB) repair pathways, i.e. nonhomologous end joining (NHEJ) and homologous recombination (HR), has been speculated. To test this possibility, we examined cells of the chicken B-lymphocyte cell line DT40 and its derivatives lacking NHEJ and/or HR: KU70(-/-), DNA-PKcs(-/-/-), RAD54(-/-) and KU70(-/-)/RAD54(-/-). Radiosensitization by hyperthermia could be seen in all of the mutants, including KU70(-/-)/RAD54(-/-), which lacked both NHEJ and HR. Therefore, radiosensitization by hyperthermia cannot be explained simply by its inhibitory effects, if any, on NHEJ and/or HR alone. However, in NHEJ-defective KU70(-/-) and DNA-PKcs(-/-/-), consisting of two subpopulations with distinct radiosensitivity, the radiosensitive subpopulation, which is considered to be cells in G(1) and early S, was not sensitized. Substantial sensitization was seen only in the radioresistant subpopulation, which is considered to be cells in late S and G(2), capable of repairing DSBs through HR. This observation did not exclude possible involvement of NHEJ in G(1) and early S phase and also suggested inhibitory effects of hyperthermia on HR. Thus partial contribution of NHEJ and HR in radiosensitization by hyperthermia, especially that depending on the cell cycle stage, remains to be considered.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0033-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
162
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
433-41
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15447039-Animals, pubmed-meshheading:15447039-B-Lymphocytes, pubmed-meshheading:15447039-Cell Line, pubmed-meshheading:15447039-Chickens, pubmed-meshheading:15447039-DNA, pubmed-meshheading:15447039-DNA Damage, pubmed-meshheading:15447039-DNA Repair, pubmed-meshheading:15447039-Dose-Response Relationship, Radiation, pubmed-meshheading:15447039-G1 Phase, pubmed-meshheading:15447039-G2 Phase, pubmed-meshheading:15447039-Hot Temperature, pubmed-meshheading:15447039-Humans, pubmed-meshheading:15447039-Hyperthermia, Induced, pubmed-meshheading:15447039-Mice, pubmed-meshheading:15447039-Recombination, Genetic, pubmed-meshheading:15447039-S Phase, pubmed-meshheading:15447039-Temperature, pubmed-meshheading:15447039-Time Factors, pubmed-meshheading:15447039-Transgenes, pubmed-meshheading:15447039-U937 Cells, pubmed-meshheading:15447039-X-Rays
pubmed:year
2004
pubmed:articleTitle
Radiosensitization by hyperthermia in the chicken B-lymphocyte cell line DT40 and its derivatives lacking nonhomologous end joining and/or homologous recombination pathways of DNA double-strand break repair.
pubmed:affiliation
Department of Radiation Research, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't