Overview
- Editors:
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Jonathan J. Li
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Division of Etiology & Prevention of Hormonal Cancers Kansas Cancer Intitute, University of Kansas Medical Center, Kansas City, USA
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Sara Antonia Li
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Division of Etiology & Prevention of Hormonal Cancers Kansas Cancer Intitute, University of Kansas Medical Center, Kansas City, USA
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Janet R. Daling
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Division of Public Health Sciences Fred Hutchinson Cancer Research Center, University of Washington, Seattle, USA
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Table of contents (59 papers)
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Front Matter
Pages i-xliii
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State of the Art Lectures
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- Jack Gorski, Tae-Yon Chun, Douglas Wendell
Pages 25-36
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- Arthur B. Pardee, Heide L. Ford, Debajit K. Biswas, Katherine J. Martin, Ruth Sager
Pages 37-43
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- Janet R. Daling, Kathleen E. Malone, Elaine A. Ostrander, Peggy L. Porter
Pages 44-58
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Epidemiology: Breast and Prostate Cancer
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- Kathleen E. Malone, Janet R. Daling, Nicola M. Suter, Kara Cushing, Thora Jonnasdottir, Elaine A. Ostrander
Pages 70-86
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Molecular Genetics of Hormonal Cancers
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- Lukas Bubendorf, Olli-P. Kallioniemi
Pages 103-112
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- C. Marcelo Aldaz, Andrzej Bednarek, April Charpentier, Michael MacLeod, Kathleen Hawkins, Kendra Laflin
Pages 113-123
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- Yvonne P. Dragan, Emile Nuwaysir, Linda Sargent, Dong-Hui Li, V. Craig Jordan, Henry C. Pitot
Pages 124-135
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Estrogen Receptor Interactions
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Front Matter
Pages 137-137
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- Jonathan J. Li, S. John Weroha, Marilyn Cansler, Sara Antonia Li
Pages 149-157
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Estrogen/Progesterone-Breast Cancer
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Front Matter
Pages 159-159
About this book
Since our previous symposium in 1995, the pace of research in hormones and cancer has accelerated. Progress in our understanding of hormonal carcinogenic processes has been a direct result of the advances made in cell biology, endocrinology, and carcinogenesis at the molecular level. The newer fields of molecular genetics and cytogenetics already have and are expected to continue to playa major role in furthering our understanding of the cellular and molecular events in hormonal carcinogenesis. It has become increasingly clear that the risk of naturally occurring sex hormones in carcinogenic processes, both in human and in animal models, requires only minute quantities of hormones, at both the serum and tissue levels. Moreover, hormone target tissues for neoplastic transformation, perhaps with the exception of the liver, generally have relatively modest ability to metabolize sex hormones, such as the breast and prostate. Table 1 summarizes the serum, and in most cases, the tissue levels of sex hormones, both endogenously and exogenously ingested, which are associated with increased risk for endocrine-associated cancers such as breast, endometrium, and prostate, as well as the hormone levels of four experimental models that have been shown to elicit high tumor incidences. In contrast to the human, in which the hormone levels are cyclic, however, the latter require continuous hormone exposure at these relatively low levels.
