Molecular and cellular pathogenesis of benign prostatic hyperplasia.
OBJECTIVE
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.


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.
Lee
Keith L
KL
Department of Urology, Stanford University School of Medicine, Stanford, California 94305-5118, USA.
Peehl
Donna M
DM
D017209:Apoptosis; D002455:Cell Division; D002478:Cells, Cultured; D016922:Cellular Senescence; D004848:Epithelium / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D008297:Male; D011470:Prostatic Hyperplasia / Q000209:etiology* / Q000235:genetics / Q000473:pathology