Cancer of the Prostate: Molecular Genetics
Molecular Biology of Specific Diseases
Published Online: 15 SEP 2006
Copyright © 2006 Wiley-VCH Verlag GmbH & Co. KGaA. All rights reserved.
Reviews in Cell Biology and Molecular Medicine
How to Cite
Dahiya, R. 2006. Cancer of the Prostate: Molecular Genetics. Reviews in Cell Biology and Molecular Medicine. .
- Published Online: 15 SEP 2006
This is not the most recent version of the article. View current version (27 JUL 2015)
Adenocarcinoma of the prostate is one of the most common cancers in men worldwide and is the second leading cause of cancer-specific death in the United States. Over the past 15 years, significant advances have been made in the treatment of prostate cancer, largely owing to earlier diagnosis and the evolution of surgical techniques and improvements in radiation therapy. Nevertheless, tremendous uncertainty and controversy exist regarding the appropriate clinical management of prostate cancer in many cases. Similarly, despite the magnitude of the problem, understanding of the pathogenesis, biology, and natural history of human prostate cancer remains incomplete and unclear. Progress has been made in the past decade in elucidating the molecular and genetic changes involved in prostate cancer development and progression. A better understanding of the underlying disease mechanisms will allow rational treatment strategies and improved outcomes. The classic model of tumor development describes a multistep process in which a series of genetic alterations leads to aberrant, uncontrolled cell growth. This is best characterized in the case of colon cancer, for which specific genetic changes have been correlated with clinical and pathologic disease progression. These genetic alterations can be both hereditary (germ-line mutation) and acquired (somatic mutation). The paradigm is less established in prostate cancer (Fig. 1). We discuss the current understanding of the molecular genetics and biology of prostate cancer development, including genetic predispositions, early changes associated with prostatic intraepithelial neoplasia (PIN), and the traditional classes of genes involved in promoting and repressing cancer development (protooncogenes/oncogenes and tumor suppressor genes, respectively). In addition, we describe recent studies on the role of genetic instability, telomerases, growth factors, cell-adhesion molecules, DNA ethylation, and the androgen receptor (AR) in prostate cancer.