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Progression of LNCaP Human Prostate Carcinoma Cells: Androgen Receptor Activity and c-myc Gene Expression

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Book cover Hormonal Carcinogenesis II

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Abstract

Prostatic carcinogenesis is a multi-step process involving progression from precancerous cells to cells that uncontrollably proliferate and metastasize. Understanding the molecular events driving the progression is critical to the early detection of and choice of treatment for prostate cancer. The growth and development of prostate cancer appears to be initially androgen-dependent, making it vulnerable to androgen ablation and anti-androgen therapies (1). However, prostate cancer cells gradually lose androgen dependency, and tumor cells which are resistant to endocrine therapy ultimately proliferate. While loss of androgen receptor (AR) expression may accompany loss of androgen dependency and responsiveness (2), other prerequisite cellular events may occur which allow cell proliferation to bypass the androgen requirement. Loss of AR expression may either drive the selection for such events or occur secondarily (3).

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Authors
  1. John M. Kokontis
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  2. Nissim Hay
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  3. Richard A. Hiipakka
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  4. Shutsung Liao
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Editor information

Editors and Affiliations

  1. Division of Etiology and Prevention of Hormonal Cancers, Hormonal Carcinogenesis Laboratory, University of Kansas Cancer Center, Kansas City, Kansas, USA

    J. Jonathan Li Ph.D. (Professor of Pharmacology, Toxicology, and Therapeutics, Director) (Professor of Pharmacology, Toxicology, and Therapeutics, Director)

  2. Hormonal Carcinogenesis Laboratory, University of Kansas Cancer Center, Kansas City, Kansas, USA

    Sara Antonia Li Ph.D. (Associate Professor of Pharmacology, Toxicology, and Therapeutics) (Associate Professor of Pharmacology, Toxicology, and Therapeutics)

  3. Department of Medical Nutrition, Center for Biotechnology, NOVUM, Huddinge University Hospital, Huddinge, Sweden

    Jan-Åke Gustafsson M.D., Ph.D. (Professor and Chairman, Director) (Professor and Chairman, Director)

  4. Department of Molecular and Cell Biology, Cancer Research Center, University of California, Berkeley, California, USA

    Satyabrata Nandi Ph.D. (Professor of Cell and Development Biology) (Professor of Cell and Development Biology)

  5. Division of Cancer Etiology, Chemical and Physical Carcinogenesis Program, National Cancer Institute, Rockville, Maryland, USA

    Lea I. Sekely Ph.D. (Program Director) (Program Director)

  6. University of Kansas Medical Center, Kansas City, Kansas, USA

    J. Jonathan Li Ph.D. (Professor of Pharmacology, Toxicology, and Therapeutics, Director) & Sara Antonia Li Ph.D. (Associate Professor of Pharmacology, Toxicology, and Therapeutics) (Professor of Pharmacology, Toxicology, and Therapeutics, Director) &  (Associate Professor of Pharmacology, Toxicology, and Therapeutics)

  7. National Institutes of Health, Rockville, Maryland, USA

    Lea I. Sekely Ph.D. (Program Director) (Program Director)

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© 1996 Springer-Verlag New York, Inc.

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Kokontis, J.M., Hay, N., Hiipakka, R.A., Liao, S. (1996). Progression of LNCaP Human Prostate Carcinoma Cells: Androgen Receptor Activity and c-myc Gene Expression. In: Li, J.J., Li, S.A., Gustafsson, JÅ., Nandi, S., Sekely, L.I. (eds) Hormonal Carcinogenesis II. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2332-0_29

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  • DOI: https://doi.org/10.1007/978-1-4612-2332-0_29

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4612-7506-0

  • Online ISBN: 978-1-4612-2332-0

  • eBook Packages: Springer Book Archive

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