## Abstract Raloxifene (RAL), a selective estrogen receptor (ER) modulator (SERM) seems to induce apoptosis in both androgen‐dependent and ‐independent prostate cell (PC) lines via activation of ERβ and an antagonistic effect on ERα. In this study, we evaluated the effects of RAL on epithelial PC g
Death receptor-induced cell death in prostate cancer
✍ Scribed by Natalya V. Guseva; Agshin F. Taghiyev; Oskar W. Rokhlin; Michael B. Cohen
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 347 KB
- Volume
- 91
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Prostate cancer mortality results from metastasis and is often coupled with progression from androgen‐dependent to androgen‐independent growth. Unfortunately, no effective treatment for metastatic prostate cancer increasing patient survival is available. The absence of effective therapies reflects in part a lack of knowledge about the molecular mechanisms involved in the development and progression of this disease. Apoptosis, or programmed cell death, is a cell suicide mechanism that enables multicellular organisms to regulate cell number in tissues. Inhibition of apoptosis appears to be a critical pathophysiological factor contributing to the development and progression of prostate cancer. Understanding the mechanism(s) of apoptosis inhibition may be the basis for developing more effective therapeutic approaches. Our understanding of apoptosis in prostate cancer is relatively limited when compared to other malignancies, in particular, hematopoietic tumors. Thus, a clear need for a better understanding of apoptosis in this malignancy remains. In this review we have focused on what is known about apoptosis in prostate cancer and, more specifically, the receptor/ligand‐mediated pathways of apoptosis as potential therapeutic targets. © 2003 Wiley‐Liss, Inc.
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