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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Communications
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- Takeki Tsutsui, Yukiko Tamura, J. C. Barrett
Pages 437-443
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- Fu-Li Yu, Mian-Ying Wang, Wanda Bender
Pages 444-450
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- Gregory A. Reed, Angela M. Wilson, Janette K. Padgitt
Pages 451-455
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- Y. C. Wong, B. Xie, S. W. Tsao
Pages 456-463
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- B. Xie, Y. C. Wong, S. W. Tsao
Pages 464-470
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- Martin Tochacek, Eric A. VanderWoude, Thomas J. Spady, Djuana M. E. Harvell, Mary C. Snyder, Karen L. Pennington et al.
Pages 471-476
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- Doris Mayer, Christel Metzger, Dirk Nehrbass, Peter Bannasch
Pages 477-483
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- John E. Coe, Kamal G. Ishak, M. J. Ross
Pages 484-488
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- Gary J. Smith, Sharon C. Presnell, William B. Coleman, Joe W. Grisham
Pages 489-495
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- Djuana M. E. Harvell, Thomas J. Spady, Tracy E. Strecker, Athena M. Lemus-Wilson, Karen L. Pennington, Fangchen Shen et al.
Pages 496-501
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- Shane T. Hentges, Dipak K. Sarkar
Pages 502-508
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- Amando Peydro-Olaya, Carmen Carda, Antonio Llombart-Bosch
Pages 509-513
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- Rajeshwar Rao Tekmal, Kiran Gill, Nameer Kirma
Pages 514-520
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- Erika Pfeiffer, Manfred Metzler
Pages 521-526
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- Sabine E. Kulling, Eric Jacobs, Manfred Metzler
Pages 527-532
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Back Matter
Pages 533-555
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.