Linked Life Data

7642467

Source:http://linkedlifedata.com/resource/pubmed/id/7642467

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-9-15
pubmed:abstractText
The study of the cellular, biochemical, and molecular biology and pharmacology of MDR has provided one of the most active and exciting areas within cancer research for translation into potential clinical benefit. Although convincing evidence for the functional role of P-gp in mediating clinical drug resistance in humans remains scant, studies of the clinical expression of P-gp and trials of chemosensitizers with cancer chemotherapy suggest "resistance modification" strategies may be effective in some tumors with intrinsic or acquired drug resistance. However, even if P-gp-associated MDR proves to be a relevant and reversible cause of clinical drug resistance, numerous problems remain to be solved before effective clinical chemosensitization may be achieved. Such factors as absorption, distribution, and metabolism, the effect of chemosensitizers on chemotherapeutic drug clearance, toxicity to normal tissues expressing P-gp, and the most efficacious modulator regimens all remain to be defined in vivo. Clearly, the identification of more specific, more potent, and less clinically toxic chemosensitizers for clinical use remains critical to the possible success of this approach. However, the finding that a number of pharmacologic agents can antagonize a well-characterized form of experimental drug resistance provides promise for potential clinical applications. Further study of chemosensitizers in humans and the rational design of novel chemosensitizers with improved activity should define the importance of MDR to clinically resistant cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0889-8588
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
337-61
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed-meshheading:7642467-Animals, pubmed-meshheading:7642467-Antineoplastic Agents, pubmed-meshheading:7642467-Biological Transport, pubmed-meshheading:7642467-Calcium Channel Blockers, pubmed-meshheading:7642467-Calmodulin, pubmed-meshheading:7642467-Cyclosporins, pubmed-meshheading:7642467-Dipyridamole, pubmed-meshheading:7642467-Drug Resistance, Multiple, pubmed-meshheading:7642467-Drug Screening Assays, Antitumor, pubmed-meshheading:7642467-Mice, pubmed-meshheading:7642467-Models, Biological, pubmed-meshheading:7642467-Molecular Structure, pubmed-meshheading:7642467-Neoplasm Proteins, pubmed-meshheading:7642467-Neoplasms, Experimental, pubmed-meshheading:7642467-P-Glycoprotein, pubmed-meshheading:7642467-Steroids, pubmed-meshheading:7642467-Structure-Activity Relationship, pubmed-meshheading:7642467-Vinca Alkaloids
pubmed:year
1995
pubmed:articleTitle
Modulators of multidrug resistance. Preclinical studies.
pubmed:affiliation
Stanford University Medical Center, Stanford University, California, USA.
pubmed:publicationType
Journal Article, Review