Nonendocrine pathways and endocrine resistance: Observations with antiestrogens and signal transduction inhibitors in combination

An increasing body of evidence demonstrates that growth factor networks are highly interactive with estrogen receptor signaling in the control of breast cancer growth. As such, tumor responses to antiestrogens are likely to be a composite of the estrogen receptor and growth factor-inhibitory activit...

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Bibliographic Details
Published in:Clinical cancer research 2004-01, Vol.10 (1), p.346s-354s
Main Authors: NICHOLSON, Robert I, HUTCHESON, Iain R, KNOWLDEN, Janice M, JONES, Helen E, HARPER, Maureen E, JORDAN, Nicola, HISCOX, Steve E, BARROW, Denise, GEE, Julia M. W
Format: Article
Language:English
Subjects:
Antineoplastic agents
Biological and medical sciences
Breast Neoplasms - metabolism
Breast Neoplasms - therapy
Cell Division
Disease Progression
Drug Resistance, Neoplasm
Endocrine Glands - metabolism
Estrogen Receptor Modulators - pharmacology
Estrogens - metabolism
Growth Substances - metabolism
Humans
Medical sciences
Pharmacology. Drug treatments
Receptor, Epidermal Growth Factor - metabolism
Receptor, IGF Type 1 - metabolism
Receptors, Estrogen - metabolism
Signal Transduction
Tamoxifen - metabolism
Tamoxifen - pharmacology
Tumors
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Summary:An increasing body of evidence demonstrates that growth factor networks are highly interactive with estrogen receptor signaling in the control of breast cancer growth. As such, tumor responses to antiestrogens are likely to be a composite of the estrogen receptor and growth factor-inhibitory activity of these agents, with alterations/aberrations in growth factor signaling providing a mechanism for the development of antiestrogen resistance. In this light, the current article focuses on illustrating the relationship between growth factor signaling and antiestrogen failure in our in-house tumor models of breast cancer and describing how we are now beginning to successfully target growth factor activity to improve the effects of antiestrogen drugs and to block aggressive disease progression.
ISSN:1078-0432
DOI:10.1158/1078-0432.CCR-031206