Abstract
Prostate cancer is the most commonly diagnosed noncutaneous cancer in men. Despite this fact, many of the genetic changes that coincide with prostate cancer progression remain enigmatic. We have addressed this problem by characterizing the expression profiles of several benign and malignant human prostate samples, and we have identified several genes that are differentially expressed between benign and malignant glands. One gene that was overexpressed encodes the serine protease hepsin. We used an independent sample set to confirm that hepsin is overexpressed in prostate tumors, and in situ hybridization demonstrates that hepsin is specifically overexpressed in the carcinoma cells themselves. These facts, together with the molecular properties of hepsin, make it an ideal target for prostate cancer therapy.
Footnotes
-
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
-
↵1 Supported by NIH Grant 5 P01 CA49712-08 and by grants from The Association for the Cure of Cancer of the Prostate (CaP CURE) and The Urological Research Foundation.
-
↵2 To whom requests for reprints should be addressed, at Division of Laboratory Medicine, Department of Pathology, Washington University School of Medicine, 660 South Euclid Avenue, Box 8118, St. Louis, MO 63110-1093. Phone: (314) 362-4650; Fax: (314) 362-8756; E-mail: jeff{at}pathbox.wustl.edu
- Received May 1, 2001.
- Accepted June 15, 2001.
- ©2001 American Association for Cancer Research.
Volume 61, Issue 15
