Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:10557052rdf:typepubmed:Citationlld:pubmed
pubmed-article:10557052lifeskim:mentionsumls-concept:C0017296lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C0007634lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C0870134lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C0037993lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C0007257lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C0600688lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C1545588lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C0681842lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C1171947lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C1513327lld:lifeskim
pubmed-article:10557052lifeskim:mentionsumls-concept:C0591833lld:lifeskim
pubmed-article:10557052pubmed:issue11lld:pubmed
pubmed-article:10557052pubmed:dateCreated1999-12-7lld:pubmed
pubmed-article:10557052pubmed:abstractTextThe effect of expression of an O6-benzylguanine (O6-beG)-resistant mutant (hATPA/GA) of human O6-alkylguanine-DNA alkyltransferase (ATase) on the in vivo toxicity and clastogenicity of the anti-tumour agent N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU) to murine bone marrow has been investigated. When compared with control animals, the bipotent granulocyte-macrophage colony-forming (GM-CFC) progenitor population of the hATPA/GA transduced mice were somewhat more resistant to BCNU (1.4-fold, P = 0.047) and this effect was more significant in the presence of the ATase inactivator O6-beG (3. 5-fold, P = 0.001). The polychromatic erythrocytes were also significantly protected against BCNU-induced clastogenicity both in the presence (P < 0.001) and absence of O6-beG (P < 0.05). The primitive, multipotent spleen colony-forming cells (CFU-S) in these animals also showed moderate (1.6-fold, P = 0.034) protection in the absence of O6-beG but in the presence of the inactivator they remained as sensitive to BCNU toxicity as those in the control animals (P = 0.133). This result contrasts with previous findings demonstrating significant hATPA/GA-mediated, O6-beG-resistant protection against the toxicity and clastogenicity of a number of O6-alkylating agents, including temozolomide, fotemustine and chlorozotocin. The possibility that our strategy for protective gene therapy may be highly agent and cell-type specific is unexpected and has possible implications for clinical trials of this approach using BCNU or related agents.lld:pubmed
pubmed-article:10557052pubmed:languageenglld:pubmed
pubmed-article:10557052pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:citationSubsetIMlld:pubmed
pubmed-article:10557052pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:10557052pubmed:statusMEDLINElld:pubmed
pubmed-article:10557052pubmed:monthNovlld:pubmed
pubmed-article:10557052pubmed:issn0887-6924lld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:RaffertyJJlld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:ThatcherNNlld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:FairbairnLLlld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:MargisonGGlld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:LashfordLLlld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:ChinnasamyNNlld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:DexterTTlld:pubmed
pubmed-article:10557052pubmed:authorpubmed-author:ChinnasamyDDlld:pubmed
pubmed-article:10557052pubmed:issnTypePrintlld:pubmed
pubmed-article:10557052pubmed:volume13lld:pubmed
pubmed-article:10557052pubmed:ownerNLMlld:pubmed
pubmed-article:10557052pubmed:authorsCompleteYlld:pubmed
pubmed-article:10557052pubmed:pagination1776-83lld:pubmed
pubmed-article:10557052pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:meshHeadingpubmed-meshheading:10557052...lld:pubmed
pubmed-article:10557052pubmed:year1999lld:pubmed
pubmed-article:10557052pubmed:articleTitleProtection of committed murine haemopoietic progenitors against BCNU toxicity does not predict protection of primitive, multipotent spleen colony-forming cells - implications for chemoprotective gene therapy.lld:pubmed
pubmed-article:10557052pubmed:affiliationCRC Sections of Genome Damage and Repair, Paterson Institute for Cancer Research, Manchester, UK.lld:pubmed
pubmed-article:10557052pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10557052pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed