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Modulation of Epidermal Growth Factor Receptor in Endocrine‐Resistant, Estrogen‐Receptor‐Positive Breast Cancer
Author(s) -
NICHOLSON R. I.,
HUTCHESON I. R.,
HARPER M. E.,
KNOWLDEN J. M.,
BARROW D.,
McCLELLAND R. A.,
JONES H. E.,
WAKELING A. E.,
GEE J.M. W.
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04101.x
Subject(s) - estrogen receptor , epidermal growth factor receptor , growth factor receptor inhibitor , cancer research , epidermal growth factor , endocrinology , medicine , breast cancer , growth factor receptor , estrogen , tyrosine kinase , endocrine system , receptor , estrogen receptor alpha , biology , cancer , hormone
A bstract : 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 antihormones are likely to be a composite of the estrogen receptor and growth factor inhibitory activity of these agents. The modulation of growth factor networks during endocrine response is examined, and in vitro and clinical evidence is presented that epidermal growth factor receptor signaling, maintained in either an estrogen receptor‐dependent or a receptor‐independent manner, is critical to antihormone‐resistant breast cancer cell growth. The considerable potential of the epidermal growth factor receptor‐selective tyrosine kinase inhibitor Iressa (ZD 1839) to efficiently treat, and perhaps even prevent, endocrine‐resistant breast cancer is highlighted.