The Biology of Antihormone Failure in Breast Cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2003-03

AUTHORS

Robert I. Nicholson, Julia M.W. Gee, Janice Knowlden, Richard McClelland, Tracie-Ann Madden, Denise Barrow, Iain Hutcheson

ABSTRACT

Many estrogen receptor-positive breast cancer patients initially respond to treatment with antihormonal agents such as tamoxifen, but remissions are often followed by acquisition of resistance and ultimately disease relapse. The development of a rationale for the effective treatment of tamoxifen-resistant breast cancer requires an understanding of the complex signal transduction mechanisms that contribute towards loss of antiestrogen response. Interactions between estrogen and growth factor signaling pathways have been identified in estrogen-responsive cells that are thought to reinforce their individual cellular effects on growth and gene responses. Increasing evidence indicates that abnormalities occurring in growth factor signaling pathways, notably the epidermal growth factor receptor (EGFR) signaling pathway, could dramatically influence steroid hormone action and may be critical to antihormonal-resistant breast cancer cell growth. Thus, inhibitory agents targeting growth factor receptors, or their intracellular pathway components, may prove clinically beneficial in antihormone refractory disease. One example, gefitinib ('Iressa', ZD1839), an EGFR-tyrosine kinase inhibitor, is an interesting therapeutic option that may provide benefit in the treatment of antihormonal-resistant breast cancer. Rapid progress with pharmacological and molecular therapeutic agents is now being made. Therapies that target growth factor signaling pathways may prevent development of resistance. More... »

PAGES

29-34

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1023/a:1025467500433

DOI

http://dx.doi.org/10.1023/a:1025467500433

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1034197538

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14535532


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