BENIGN HYPERPLASIA AND CANCER OF THE PROS TATE - STEROID-HORMONES ANDGROWTH-FACTORS

Citation
S. Chevalier et al., BENIGN HYPERPLASIA AND CANCER OF THE PROS TATE - STEROID-HORMONES ANDGROWTH-FACTORS, MS. Medecine sciences, 9(5), 1993, pp. 542-546
Citations number
NO
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
07670974
Volume
9
Issue
5
Year of publication
1993
Pages
542 - 546
Database
ISI
SICI code
0767-0974(1993)9:5<542:BHACOT>2.0.ZU;2-S
Abstract
Statistics concerning the incidence of benign prostatic hyperplasia an d cancer in industrialized countries are alarming : between 50 and 80 years of age, 50 % to 90 % of men develop an hyperplastic prostate and 30 % of them will have to undergo surgery ; moreover, one man out of eleven suffers from prostate cancer and the chances of cure, even with the most advanced endocrine therapies, are limited. This is mainly du e to the fact that the relapse of most tumors is caused by androgen-in dependent cell proliferation. In the present review, we will consider androgen-dependent and -independent prostatic epithelial cells, with r espect to the actual therapies used for prostate cancer and regarding the fundamental questions now being addressed in the field of prostate physiopathology. The beneficial effects of castration and of estrogen administration observed in the forties were the basis of the endocrin e therapies in current use. Chemical castration with LH-RH analogs is gradually replacing surgical castration while anti-androgens and inhib itors of 5alpha-reductase are administered to prevent, respectively, t he binding of hormones, including adrenal androgens, to their specific receptors and the formation of the active metabolite, dihydrotestoste rone. Up to now, investigators have failed to correlate androgen recep tors with the response of patients to endocrine therapies. Further stu dies at the molecular level are required to understand the mechanisms underlying hormone dependency or independency. The major problem of tu mor relapse after endocrine therapies remains unsolved and limits the clinicians to non-specific treatments such as radio- and chemotherapie s. It has led to a whole new field of fundamental research related to prostate growth, namely on the role of prostatic stroma, genetic rearr angement, rate of cell death and, particularly, on the role of known g rowth factors and/or of novel prostatic factors as well as their recep tors and related protein-tyrosine-kinases and oncogenes. These avenues appear very promising. There is more and more indications that these research efforts will lead to the development of new diagnostic method s and of specific therapies in the near future.