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Titolo:
Role of transforming growth factor-beta 1 in prostate cancer
Autore:
Wikstrom, P; Damber, JE; Bergh, A;
Indirizzi:
Umea Univ, Dept Surg & Perioperat Sci, SE-90185 Umea, Sweden Umea Univ Umea Sweden SE-90185 g & Perioperat Sci, SE-90185 Umea, Sweden Sahlgrenska Univ Hosp, Dept Urol, Inst Surg Diciplines, SE-41345 Gothenburg, Sweden Sahlgrenska Univ Hosp Gothenburg Sweden SE-41345 1345 Gothenburg, Sweden Umea Univ, Dept Med Biosci, SE-90185 Umea, Sweden Umea Univ Umea Sweden SE-90185 v, Dept Med Biosci, SE-90185 Umea, Sweden
Titolo Testata:
MICROSCOPY RESEARCH AND TECHNIQUE
fascicolo: 4, volume: 52, anno: 2001,
pagine: 411 - 419
SICI:
1059-910X(20010215)52:4<411:ROTGF1>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT VENTRAL PROSTATE; PROGRAMMED CELL-DEATH; TGF-BETA RECEPTOR; CASTRATION-INDUCED INVOLUTION; EPITHELIAL-CELLS; STROMAL CELLS; TUMOR-SUPPRESSOR; CARCINOMA-CELLS; II RECEPTORS; GROWTH-FACTOR-BETA-1 TGF-BETA-1;
Keywords:
TGF-beta 1; regulation of prostatic growth; angiogenesis; metastasis; immunosuppression;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
107
Recensione:
Indirizzi per estratti:
Indirizzo: Wikstrom, P Umea Univ, Dept Surg & Perioperat Sci, SE-90185 Umea, Sweden Umea Univ Umea Sweden SE-90185 at Sci, SE-90185 Umea, Sweden
Citazione:
P. Wikstrom et al., "Role of transforming growth factor-beta 1 in prostate cancer", MICROSC RES, 52(4), 2001, pp. 411-419

Abstract

TGF-beta1 is an important regulator of the normal and malignant prostate. In the non-malignant prostate, TGF-beta1 stimulates cell differentiation, inhibits epithelial cell proliferation, and induces epithelial cell death. TGF-beta1 is secreted into semen where it is an important immunosuppressive factor. Prostate cancer cells express high levels of TGF-beta1, which seemsto enhance prostate cancer growth and metastasis by stimulating angiogenesis and by inhibiting immune responses directed against tumour cells. Prostate cancer cells frequently lose their TGF-beta receptors and acquire resistance to the anti-proliferative and pro-apoptotic effects of TGF-beta1. Accordingly, high expression of TGF-beta1 and loss of TGF-beta receptor expression have been associated with a particularly bad prognosis in human prostate cancer patients. TGF-beta1 also seems to be a mediator of castration-induced apoptosis in androgen dependent normal and malignant prostate epithelial cells. The ability of some prostate tumours to avoid castration-induced apoptosis may not, however, be simply due to loss of TGF-beta receptor type I or type II expression in the tumour cells. It may also be related to an inability of these cells to up-regulate TGF-beta receptor levels in responseto castration or possibly due to defects downstream of the receptors. Short-term therapy-induced changes in the TGF-beta system in prostate tumours can probably be used to predict the long-term response to androgen ablation treatment. Further investigations into the TGF-beta system in the prostate are needed, however, to elucidate how alterations in this system affect thebehaviour of prostate tumours, and whether this system can be manipulated for therapeutical purposes. Microsc. Res. Tech. 52:411-419, 2001. 2001 Wiley-Liss, Inc.

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Documento generato il 07/04/20 alle ore 03:51:34