Linked Life Data

11182049

Source:http://linkedlifedata.com/resource/pubmed/id/11182049

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Therapeutic strategies for patients with advanced-stage adenocarcinoma of the breast frequently include the use of cytotoxic chemotherapy. Insulin-like growth factor I (IGF-I) receptor, a key factor in cell-cycle regulation, is frequently overexpressed in high-grade breast cancers. IGF-I receptor overexpression in these tumors may provide a target for novel molecular therapy against this disease. Early passage samples of estrogen-responsive (ER+) MCF 7 and estrogen receptor-negative (ER-) MDA-231 cells were cultured in semi-confluent conditions. Dose-titrations were performed for doxorubicin and taxol with receptor modulation using IGF-I or a competitive receptor inhibitor, alphaIR3. The addition of 100 ng/ml IGF-I resulted in a >2-fold mitogenic response in both ER+ and ER- cells. Receptor activation prior to the treatment with cytotoxic chemotherapeutic agents altered the pattern of response with a 26.3% increase in IC50. Doxorubicin and taxol both produced dose-related toxicity with IC50 of 0.05 microg/ml and 0.00 microg/ml respectively. The addition of alphaIR3 resulted in increased cytotoxicity in IGF-I stimulated cells compared with the use of doxorubicin or taxol alone. These results suggest that IGF-I receptor modulation alters the response to cytotoxic chemotherapeutic agents in breast cancer cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1021-335X
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
325-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:articleTitle
Insulin-like growth factor-I receptor antagonism results in increased cytotoxicity of breast cancer cells to doxorubicin and taxol.
pubmed:affiliation
University of Tennessee-Memphis College of Medicine, Department of Surgery/Surgical Oncology, Memphis, TN 38163, USA. dbeech@utmem.edu
pubmed:publicationType
Journal Article, Comparative Study