Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
1998-11-18
pubmed:abstractText
The emergence of drug resistance to chemotherapeutic agents is a major cause of treatment failure in cancer therapy. Therefore, much effort has been aimed at circumventing or reversing this undesired effect. Recently, we found that tumor cell lines selected for their multidrug-resistant phenotype can also exhibit increased levels of TAP mRNA and MHC class I proteins. This raised the question of whether drug-resistant tumors are more readily recognized by MHC-restricted CTLs. In this report, we show that five of five MHC class I+ tumor cell lines grown in medium containing Adriamycin developed into variants that expressed higher levels of MHC class I than did their corresponding parental cell lines. This was not observed with a MHC class I- cell line. No similar association was noted for changes in the expression of either HER-2 or intercellular adhesion molecule 1 protein. We also found that MHC class I+ drug-selected variants were more readily lysed by MHC-restricted, tumor-associated CTLs than were the drug-sensitive parental cell lines. When the drug-selected variants were cocultured with the same CTLs to eliminate tumor cells expressing higher levels of MHC-I (MHC-Ihi), the CTL-resistant tumor cells exhibited a drug sensitivity profile similar to that of the parental cell lines that were not exposed to Adriamycin. These findings suggest that certain chemotherapeutic drugs may increase the immunogenicity of some tumors, and that CTL immunotherapy may help reverse drug resistance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4790-3
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Increased sensitivity of adriamycin-selected tumor lines to CTL-mediated lysis results in enhanced drug sensitivity.
pubmed:affiliation
Department of Gynecologic Oncology, The University of Texas M. D. Anderson Cancer Center, and The University of Texas Medical School-Houston, 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.