Differential expression of steroid receptors in prostate tissues before and after radiation therapy for prostatic adenocarcinoma

✍ Scribed by Emina Torlakovic; Wolfgang Lilleby; Aasmund Berner; Goran Torlakovic; Rajni Chibbar; Torbjørn Furre; Sophie D. Fosså

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: French
• Weight: 272 KB
• Volume: 117
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.21174

✦ Synopsis

Abstract

The expression, distribution and the role of steroid receptors in benign and malignant untreated prostate tissues is well recognized, however, the status of steroid receptors in prostate after radiotherapy (RT) for adenocarcinoma has not yet been studied fully. Immunohistochemical evaluation of androgen receptor (AR), estrogen receptor‐alpha (ER‐α), estrogen receptor‐beta (ER‐β), and progesterone receptor (PR) was carried out in prostate needle biopsies obtained before and after radiotherapy from 60 patients with adenocarcinoma. The ER‐β transcripts were also studied by RT‐PCR in LNCaP prostate carcinoma cell line before and 24 hr after γ‐irradiation at 0.5 Gy and 8.0 Gy. Significantly higher level of ER‐β expression was found in post‐radiation samples of prostate adenocarcinoma and benign epithelium. After RT, all steroid receptors were upregulated in prostatic stroma. Tumor AR expression did not change significantly. Although a positive association between AR and ER‐β expression was observed in pre‐treatment prostate adenocarcinoma, it was lost after RT suggesting that these 2 steroid receptors respond differently to RT. High levels of pretreatment tumor ER‐β were associated with local recurrence after RT and decreased biochemical recurrence‐free survival (p = 0.028). LNCaP cell line that expressed no ER‐β mRNA before γ‐irradiation, clearly expressed ER‐β mRNA 24 hr after 0.5 Gy and 8.0 Gy. Upregulation of all steroid receptors in the prostate stroma and upregulation of ER‐β in the tumor epithelium after RT, may represent a protective tissue response to radiation‐induced tissue injury. Although stromal AR was doubled after RT, the tumor and benign epithelium expression of AR seemed resistant to change by RT. © 2005 Wiley‐Liss, Inc.