Linked Life Data

3399900

Source:http://linkedlifedata.com/resource/pubmed/id/3399900

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4866
pubmed:dateCreated
1988-9-8
pubmed:abstractText
Drug resistance represents a major obstacle to successful cancer chemotherapy. However, the specific biochemical mechanisms responsible for clinical drug resistance are unknown. In these studies resistance to the antitumor agent adriamycin was found to involve two mechanisms, one that decreased drug accumulation by the P170 mechanism and another that altered the glutathione redox cycle, an important pathway in the detoxification of reactive oxygen. This dual mechanism of drug resistance was demonstrated in cell lines that had acquired the multidrug-resistant phenotype and in human colorectal cancer cells with de novo resistance. These studies support a model of acquired and de novo multidrug resistance that includes alterations in both drug accumulation and the glutathione redox cycle.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
241
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
694-7
pubmed:dateRevised
2007-3-19
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Role of the glutathione redox cycle in acquired and de novo multidrug resistance.
pubmed:affiliation
Joint Center for Radiation Therapy, Harvard Medical School, Boston, MA 02115.
pubmed:publicationType
Journal Article