Resistance to apoptosis and up regulation of Bcl-2 in benign prostatic hyperplasia after androgen deprivation

The Journal of Urology
M CardilloE P Gelmann

Abstract

Benign prostatic hyperplasia (BPH) is related to advancing age and the presence of androgens and occurs in virtually all older men. BPH causes morbidity, most often by urinary obstruction, in a substantial fraction of men over sixty. Both finasteride and androgen ablation induce partial diminution in BPH that occurs over weeks to months. This is in contrast to the often rapid involution seen in both normal prostatic epithelium and prostatic carcinoma in response to androgen withdrawal. This study was performed to analyze the response of prostatic cells, and in particular BPH, to acute androgen ablation. We subjected a cohort of 26 men to androgen ablation with goserelin, a gonadotrophin releasing hormone agonist, for 3-4 weeks prior to radical prostatectomy for prostate cancer. Preablation biopsy specimens and prostatectomy specimens were immunohistochemically stained for apoptotic cells and for expression of apoptosis regulatory proteins Bcl-2, Bax, Bcl-x, and Bak. Normal prostatic epithelial cells and prostate cancer responded to hormone deprivation by undergoing apoptosis, but in 19/26 specimens prostatic hyperplasia had a total absence of apoptosis. In all 26 specimens, benign prostatic hyperplasia demonstrated increased ex...Continue Reading

References

Oct 22, 1992·The New England Journal of Medicine·G J GormleyJ S Tenover
Nov 1, 1990·British Journal of Urology·D R JonesW B Peeling
Feb 1, 1991·The Journal of Urology·A W PartinP C Walsh
Jul 1, 1989·The Journal of Urology·M YokoyamaM Takeuchi
Aug 17, 1989·The New England Journal of Medicine·E D CrawfordP J Goodman
Sep 1, 1984·The Journal of Urology·S J BerryL L Ewing
Nov 15, 1984·The New England Journal of Medicine·UNKNOWN Leuprolide Study Group
Mar 1, 1995·British Journal of Urology·M Caine
Apr 20, 1995·Nature·T ChittendenB C Guild
Sep 27, 1994·Proceedings of the National Academy of Sciences of the United States of America·T SatoH G Wang
Jan 1, 1994·The Journal of Cell Biology·J C Reed
Sep 1, 1953·The Journal of Urology·W W SCOTT

❮ Previous
Next ❯

Citations

Dec 8, 1998·International Journal of Cancer. Journal International Du Cancer·M FiorentinoW F Grigioni
Mar 6, 2009·Acta Pharmacologica Sinica·Mayumi SuzukiShizuo Yamada
Jan 5, 2000·BJU International·S J Foley, D M Bailey
Oct 10, 2006·Clinical Genitourinary Cancer·Krisha J OpfermannJeffrey D Forman
Oct 12, 2005·The Journal of Urology·Shahrokh F ShariatYair Lotan
Nov 17, 1998·The Journal of Urology·A M De MarzoD S Coffey
Mar 30, 2017·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Isha RaniNavneet Agnihotri
Nov 1, 2000·The Prostate. Supplement·T C Thompson, G Yang
Sep 25, 2003·International Journal of Cancer. Journal International Du Cancer·Stanislav ZelivianskiMing-Fong Lin
Dec 24, 2002·Prostate Cancer and Prostatic Diseases·A De La TailleD Chopin
Dec 24, 2002·Prostate Cancer and Prostatic Diseases·C A RothermundJ K Vishwanatha
Sep 24, 2004·Journal of Medicinal Food·Eun-Sun Hwang, Phyllis E Bowen

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis