Symptomatic and asymptomatic benign prostatic hyperplasia: Molecular differentiation by using microarrays

  1. Kulkarni Prakash*,
  2. Gregorio Pirozzi*,
  3. Michael Elashoff*,
  4. William Munger*,
  5. Iwao Waga,
  6. Rajiv Dhir,
  7. Yoshiyuki Kakehi§, and
  8. Robert H. Getzenberg,
  1. *Gene Logic Inc., 708 Quince Orchard Road, Gaithersburg, MD 20878; Departments of Urology, Pathology, and Pharmacology, and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, 200 Lothrop Street, Pittsburgh, PA 15213; Japan Tobacco Inc., Pharmaceutical Frontier Research Laboratories, 13-2, Fukura 1-chrome, Kanazawa-Ku, Yokahama, Kanagawa 236-0004, Japan; and §Department of Urology, Kagawa Medical University, Oaza Ikenobe, Miki-cho, Kida-gun, Kagawa 761-0793, Japan
  1. Communicated by Sherman M. Weissman, Yale University School of Medicine, New Haven, CT (received for review December 5, 2001)

Abstract

Benign prostatic hyperplasia (BPH) is a disease of unknown etiology that significantly affects the quality of life in aging men. Histologic BPH may present itself either as symptomatic or asymptomatic in nature. To elucidate the molecular differences underlying BPH, gene expression profiles from the prostate transition zone tissue have been analyzed by using microarrays. A set of 511 differentially expressed genes distinguished symptomatic and asymptomatic BPH. This genetic signature separates BPH from normal tissue but does not seem to change with age. These data could provide novel approaches for alleviating symptoms and hyperplasia in BPH.

Footnotes

  • To whom reprint requests should be addressed at: Shadyside Medical Center, Suite G40, 5200 Center Avenue, Pittsburgh, PA. E-mail: getzenbergrh{at}msx.upmc.edu.

  • Abbreviations:
    BPH,
    benign prostatic hyperplasia;
    PCA,
    principal component analysis;
    EST,
    expressed sequence tag
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