Caspase 3 expression in benign prostatic hyperplasia and prostate carcinoma

被引:46
作者
O'Neill, AJ
Boran, SA
O'Keane, C
Coffey, RNT
Hegarty, NJ
Hegarty, P
Gaffney, EF
Fitzpatrick, JM
Watson, RWG
机构
[1] Univ Coll Dublin, Mater Misericordiae Hosp, Dept Surg, Conway Inst Biomol & Biomed Res, Dublin 7, Ireland
[2] Univ Coll Dublin, Mater Misericordiae Hosp, Dept Histopathol, Dublin 7, Ireland
[3] St Jamess Univ Hosp, Dept Histopathol, Dublin, Ireland
关键词
apoptosis; caspase; 3; immunohistochemistry; prostate;
D O I
10.1002/pros.1061
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND. Apoptotic resistance to androgen ablation represents a significant problem in the treatment of prostate cancer. Over expression of antiapoptotic proteins such as Bcl-2 and mutations in p53 contribute to this resistance. The caspase family of proteases are central executioners of the cell death pathway. They are expressed in normal prostate secretory epithelial cells. Altered expression may represent an additional component leading to cell resistance. The aim of this study was to determine by immunohistochemistry caspase 3 expression in benign prostatic hyperplasia and prostate cancers. METHODS. Twenty-two patients with histologically determined prostate cancer and benign prostatic hyperplasia (BPH) were investigated. All specimens were obtained from patients undergoing surgical resection of the prostate. Immunohistochemical analysis was performed on formalin fixed paraffin embedded sections to assess caspase 3 expression. RESULTS. Caspase 3 was expressed in 18/22 (81.1%) samples, with high expression in BPH which demonstrated staining in both basal and secretory epithelial cells. Increasing grades of prostatic cancer showed a significant loss of expression in secretory epithelial layers and little staining in epithelial cells in high-grade prostatic carcinoma. CONCLUSIONS. Altered caspase 3 expression may represent an additional mechanism of apoptotic resistance to androgen ablation. Prostate 47:183-188, 2001. (C) 2001 Wiley-Liss, Inc.
引用
收藏
页码:183 / 188
页数:6
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