Linked Life Data

12517538

Source:http://linkedlifedata.com/resource/pubmed/id/12517538

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-1-8
pubmed:abstractText
Tumour resistance and dose-limiting toxic effects restrict treatment with most chemotherapeutic drugs. Elucidation of the mechanisms of these effects could permit the development of ways to improve the effectiveness of currently used agents until better therapeutic agents are developed. Several types of alkylating agents are used in the treatment of cancer. The DNA repair protein, O6-alkylguanine-DNA alkyltransferase (ATase) is an important cellular resistance mechanism to one class of alkylating agents. This enzyme removes potentially lethal damage from DNA and experiments in vitro and in vivo have shown that its inactivation can reverse resistance to such agents. Clinical trials of drugs that inactivate ATase are underway and early results indicate that they are active in tumour tissues. However, the ATase present in normal tissues, particularly bone marrow, is also inactivated, necessitating a reduction in the dose of alkylating agent. An important question is whether, in the absence of any tumour-specific delivery strategy, such drugs will improve therapeutic effectiveness; initial reports are not promising.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1470-2045
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
37-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Improvement of chemotherapy efficacy by inactivation of a DNA-repair pathway.
pubmed:affiliation
Cancer Research UK Medical Oncology Unit, Churchill Hospital, Oxford, UK.
pubmed:publicationType
Journal Article, Review