Molecular and cellular pathogenesis of benign prostatic hyperplasia

被引:150
作者
Lee, KL [1 ]
Peehl, DM [1 ]
机构
[1] Stanford Univ, Ctr Med, Dept Urol, Sch Med, Stanford, CA 94305 USA
关键词
prostate; prostatic hyperplasia;
D O I
10.1097/01.ju.0000133655.71782.14
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Purpose: Symptomatic benign prostatic hyperplasia (BPH) is one of the most common ailments seen by the urologist. Significant advances have occurred in medical and surgical therapy, and in the understanding of the biology of this disease. However, the basic science literature is often conflicting and confusing, without a unified voice. We report the current state of knowledge of the molecular and cellular basis of BPH. Materials and Methods: We compiled and interpreted basic science studies relevant to BPH pathogenesis. Results: Cellular alterations that include changes in proliferation, differentiation, apoptosis and senescence in the epithelium and stroma are implicated in BPH pathogenesis. Molecular analyses have yielded numerous candidate genes important in disease progression. Differential expression of cytokines and growth factors in BPH tissue suggests roles for inflammation and hypoxia. Through the use of cell culture models the complex regulatory mechanisms of growth control in BPH are becoming defined. Conclusions: The scientific endeavor has resulted in great strides in our understanding of BPH on a molecular and cellular level. It is hopeful that basic science and translational research will improve treatment and prevention strategies for this common disease of elderly men.
引用
收藏
页码:1784 / 1791
页数:8
相关论文
共 90 条
[11]  
BONKHOFF H, 1993, VERH DEUT G, V77, P31
[12]  
Bonkhoff H, 1998, PROSTATE, P18
[13]   THE PROLIFERATIVE FUNCTION OF BASAL CELLS IN THE NORMAL AND HYPERPLASTIC HUMAN PROSTATE [J].
BONKHOFF, H ;
STEIN, U ;
REMBERGER, K .
PROSTATE, 1994, 24 (03) :114-118
[14]   BENIGN PROSTATIC HYPERPLASIA AND NORMAL PROSTATE AGING - DIFFERENCES IN TYPE-I AND TYPE-II 5-ALPHA-REDUCTASE AND STEROID-HORMONE RECEPTOR MESSENGER-RIBONUCLEIC-ACID (MESSENGER-RNA) LEVELS, BUT NOT IN INSULIN-LIKE GROWTH-FACTOR MESSENGER-RNA LEVELS [J].
BONNET, P ;
REITER, E ;
BRUYNINX, M ;
SENTE, B ;
DOMBROWICZ, D ;
DELEVAL, J ;
CLOSSET, J ;
HENNEN, G .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1993, 77 (05) :1203-1208
[15]   Secretion of insulin-like growth factors and their binding proteins by human normal and hyperplastic prostatic cells in primary culture [J].
Boudon, C ;
Rodier, G ;
Lechevallier, E ;
Mottet, N ;
Barenton, B ;
Sultan, C .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1996, 81 (02) :612-617
[16]  
BRAWER MK, 1985, CANCER RES, V45, P3663
[17]   Cellular senescence in the pathogenesis of benign prostatic hyperplasia [J].
Castro, P ;
Giri, D ;
Lamb, D ;
Ittmann, M .
PROSTATE, 2003, 55 (01) :30-38
[18]   Expression of senescence-associate beta-galactosidase in enlarged prostates from men with benign prostatic hyperplasia [J].
Choi, J ;
Shendrik, I ;
Peacocke, M ;
Peehl, D ;
Buttyan, R ;
Ikeguchi, EF ;
Katz, AE ;
Benson, MC .
UROLOGY, 2000, 56 (01) :160-166
[19]   Cell kinetic in epithelium and stroma of benign prostatic hyperplasia [J].
Claus, S ;
Berges, R ;
Senge, T ;
Schulze, H .
JOURNAL OF UROLOGY, 1997, 158 (01) :217-221
[20]   RELATIONSHIP OF NEUROENDOCRINE CELLS OF PROSTATE AND SEROTONIN TO BENIGN PROSTATIC HYPERPLASIA [J].
COCKETT, ATK ;
DISANTAGNESE, PA ;
GOPINATH, P ;
SCHOEN, SR ;
ABRAHAMSSON, PA .
UROLOGY, 1993, 42 (05) :512-519