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Vol. 53, Issue 1, 25-72, March 2001
Vincent T. Lombardi Cancer Center, Georgetown University School of
Medicine, Washington, DC
I. Introduction
A. Role of Estrogens in Affecting Breast Cancer Risk and
Progression
B. Antiestrogens: Partial Agonists and Antagonists
C. Response Rates to Tamoxifen and Expression of Steroid Hormone
Receptors
D. Overview of Antiestrogen Resistance Mechanisms
II. Endogenous and Exogenous Estrogens in Antiestrogen Resistance
A. Origins of Intratumor Estrogens
B. Intratumor Estrogen Concentrations
C. Does the Pituitary-Ovarian Axis Affect Response to Tamoxifen in
Premenopausal Women?
D. Can Endogenous Estrogens or Hormone Replacement Therapies
Produce Antiestrogen Resistance?
III. Pharmacokinetics in Resistance to Tamoxifen
A. Basic Pharmacology of Tamoxifen
B. Intracellular Antiestrogen Binding Sites
C. Binding to Plasma Membranes
D. Altered Drug Accumulation/Transport and P-glycoprotein
(mdr1)
E. Metabolism and Resistance
F. Comments
IV. Cell Culture Models of Antiestrogen Responsiveness and
Resistance
A. R27 and LY2
B. MCF-7RR
C. The LCC Series
D. ZR-75-9a1
E. Resistance Phenotypes Implied by Cell Culture Models
V. Tamoxifen-Stimulated Proliferation as a Resistance Mechanism
A. In Vivo Selection against Tamoxifen or ICI 182,780
B. MCF-WES and MCF/TOT
C. Fibroblast Growth Factor-Transfected MCF-7 Variants and Their
Role(s) in Antiestrogen Resistance
D. Angiogenesis and Tamoxifen Resistance
E. Tamoxifen Stimulation as a Resistance Phenotype in Patients and
Tamoxifen Flare
VI. Estrogen Receptors, Mutant Receptors, Coregulators, and Gene
Networks
A. Wild-Type and Mutant Estrogen Receptor-
and Estrogen
Receptor-
B. Coregulators of Estrogen Receptor Action
C. Estrogenic and Antiestrogenic Regulation of Mitogen-Activated
Protein Kinase
D. Regulation of Gene Networks by Receptor Cross-Talk:
Mitogen-Activated Protein Kinase Activation and Estrogen Receptor
Function
E. Mitogen-Activated Protein Kinases in Mediating the Effects of
Estrogens and Conferring Antiestrogen Resistance
F. Estrogen Receptor Signaling through AP-1 and Antiestrogen
Resistance
G. Signaling to Mitogenesis or Apoptosis in Antiestrogen Resistance
VII. Growth Factors as Mediators of Antiestrogen Resistance
A. Gene Networks: Growth Factors, Their Receptors, and Cellular
Signaling
B. Epidermal Growth Factor, Transforming Growth Factor-, and
Other Family Members
C. Epidermal Growth Factor-Receptor and c-erb-B2
D. Tranforming Growth Factor- Family
E. Insulin-Like Growth Factors, Their Receptors, and Binding
Proteins
VIII. Estrogen Receptor-Independent Targets for Mediating
Antiestrogen Action and Resistance
A. Oxidative Stress
B. Perturbations in Membrane Structure/Function
C. Protein Kinase C
D. Calmodulin
E. Comments on the Possible Role of Nongenomic Effects
IX. Immunologic Mechanisms of Tamoxifen Resistance
A. Cell-Mediated Immunity
B. Natural Killer Cells
C. Macrophages
D. Lymphokine-Activated Killer Cells, Cytotoxic T Cells, and Other
Cell-Mediated Immunity Effector Cells
E. Humoral Immunity
X. Conclusions and Future Prospects
Acknowledgments
References
Antiestrogen therapy remains one of the most widely used and
effective treatments for the management of endocrine responsive breast
cancers. This reflects the ability of antiestrogens to compete with
estrogens for binding to estrogen receptors. Whereas response rates of
up to 70% are reported in patients with tumors expressing estrogen and
progesterone receptors, most responsive tumors will eventually acquire
resistance. The most important factor in de novo resistance is lack of
expression of these receptors. However, the mechanisms driving
resistance in tumors that express estrogen and/or progesterone
receptors are unclear. A tamoxifen-stimulated phenotype has been
described, but seems to occur only in a minority of patients. Most
tumors (>80%) may become resistant through other, less well defined,
resistance mechanisms. These may be multifactorial, including changes
in immunity, host endocrinology, and drug pharmacokinetics. Significant
changes within the tumor cells may also occur, including alterations in
the ratio of the estrogen receptor : forms and/or other changes
in estrogen receptor-driven transcription complex function. These may
lead to perturbations in the gene network signaling downstream of
estrogen receptors. Cells may also alter paracrine and autocrine
growth factor interactions, potentially producing a ligand-independent
activation of estrogen receptors by mitogen-activated protein kinases.
Antiestrogens can affect the function of intracellular proteins and
signaling that may, or may not, involve estrogen receptor-mediated
events. These include changes in oxidative stress responses, specific
protein kinase C isoform activation, calmodulin function, and cell
membrane structure/function.
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J. M. Knowlden, I. R. Hutcheson, H. E. Jones, T. Madden, J. M. W. Gee, M. E. Harper, D. Barrow, A. E. Wakeling, and R. I. Nicholson Elevated Levels of Epidermal Growth Factor Receptor/c-erbB2 Heterodimers Mediate an Autocrine Growth Regulatory Pathway in Tamoxifen-Resistant MCF-7 Cells Endocrinology, March 1, 2003; 144(3): 1032 - 1044. [Abstract] [Full Text] [PDF]
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Y. H. Ju, D. R. Doerge, K. F. Allred, C. D. Allred, and W. G. Helferich Dietary Genistein Negates the Inhibitory Effect of Tamoxifen on Growth of Estrogen-dependent Human Breast Cancer (MCF-7) Cells Implanted in Athymic Mice Cancer Res., May 1, 2002; 62(9): 2474 - 2477. [Abstract] [Full Text] [PDF]
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M. V. Karamouzis, V. G. Gorgoulis, and A. G. Papavassiliou Transcription Factors and Neoplasia: Vistas in Novel Drug Design Clin. Cancer Res., May 1, 2002; 8(5): 949 - 961. [Abstract] [Full Text] [PDF]
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