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Titolo:
Amplification of the androgen receptor may not explain the development of androgen-independent prostate cancer
Autore:
Edwards, J; Krishna, NS; Mukherjee, R; Watters, AD; Underwood, MA; Bartlett, JMS;
Indirizzi:
Univ Glasgow, Glasgow Royal Infirm, Dept Surg, Glasgow G31 2ER, Lanark, Scotland Univ Glasgow Glasgow Lanark Scotland G31 2ER ow G31 2ER, Lanark, Scotland Univ Glasgow, Glasgow Royal Infirm, Dept Urol, Glasgow G31 2ER, Lanark, Scotland Univ Glasgow Glasgow Lanark Scotland G31 2ER ow G31 2ER, Lanark, Scotland
Titolo Testata:
BJU INTERNATIONAL
fascicolo: 6, volume: 88, anno: 2001,
pagine: 633 - 637
SICI:
1464-4096(200110)88:6<633:AOTARM>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
IN-SITU HYBRIDIZATION; GENE AMPLIFICATION; ANTIGEN GENE; CROSS-TALK; PROGRESSION; PROTEIN; EXPRESSION; CARCINOMA; INDUCTION; BLOCKADE;
Keywords:
prostate cancer; androgen receptor; X chromosome; fluorescence in situ hybridization;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
17
Recensione:
Indirizzi per estratti:
Indirizzo: Edwards, J Univ Glasgow, Glasgow Royal Infirm, Dept Surg, Level II,Queen Elizabeth Bldg, Glasgow G31 2ER, Lanark, Scotland Univ Glasgow Level II,Queen Elizabeth Bldg Glasgow Lanark Scotland G31 2ER
Citazione:
J. Edwards et al., "Amplification of the androgen receptor may not explain the development of androgen-independent prostate cancer", BJU INT, 88(6), 2001, pp. 633-637

Abstract

Objective To examine the role of androgen receptor (AR) gene amplificationand aneusomy of the X chromosome in the development of antiandrogen-resistant prostate cancer. Patients and methods Twenty patients with prostate cancer resistant to androgen-deprivation therapy were selected for study. The records of patients with tumours before and after antiandrogen therapy, and with a full clinical follow-up, were retrieved. AR gene amplification and X chromosome copy number were assessed by fluorescence in situ hybridization using a labelled probe at locus Xq11-13 for the AR gene and a labelled a-satellite probe for the X chromosome. At least 20 nuclei were scored over three tumour areas bytwo independent observers. Results Aneusomy of the X chromosome was reported respectively in seven (35%) and 11 (55%) tumours before and after hormone relapse, the AR gene copynumber was increased in seven (35%) and 13 (65%), respectively, and AR gene amplification was detected in one (5%) and three (15%), respectively. Neither increased AR copy number nor AR amplification in primary tumours precluded a biological response to androgen-deprivation therapy. Conclusion The rate of AR gene amplification is too low to be solely responsible for the development of antiandrogen-resistant prostate cancer. Also,the presence of amplified AR and cells aneusomic for the X chromosome in primary tumours that respond to androgen-deprivation therapy suggests that an increase in AR gene copy number does not prevent a tumour from respondingto this therapy. Therefore other mechanisms which could cause hormone-refractory prostate cancer must be investigated before it is understood why so many patients relapse with this disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 11:43:41