1998
DOI: 10.1002/(sici)1097-0215(19980518)76:4<506::aid-ijc11>3.0.co;2-5
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Growth-inhibitory effects of luteinizing hormone-releasing hormone (LHRH) agonists on xenografts of the DU 145 human androgen-independent prostate cancer cell line in nude mice

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Cited by 90 publications
(139 citation statements)
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“…The presence of these receptors enables LHRH analogues to affect directly prostate tumour cells (Qayum et al, 1990;Halmos et al, 2000) in addition to the indirect central androgen suppression. In addition, it has been shown that LHRH agonists directly inhibit cell proliferation of DU-145 and LNCaP prostate cancer cell lines (Dondi et al, 1994Limonta et al, 2001). In line with these observations, the LHRH analogue Cetrorelix has been shown to have direct antiproliferative actions on DU-145 cells (Jungwirth et al, 1997b).…”
mentioning
confidence: 71%
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“…The presence of these receptors enables LHRH analogues to affect directly prostate tumour cells (Qayum et al, 1990;Halmos et al, 2000) in addition to the indirect central androgen suppression. In addition, it has been shown that LHRH agonists directly inhibit cell proliferation of DU-145 and LNCaP prostate cancer cell lines (Dondi et al, 1994Limonta et al, 2001). In line with these observations, the LHRH analogue Cetrorelix has been shown to have direct antiproliferative actions on DU-145 cells (Jungwirth et al, 1997b).…”
mentioning
confidence: 71%
“…This subline is highly invasive in response to upregulation of autocrine EGFR signalling (Xie et al, 1995;Turner et al, 1996) that exists in practically all prostate carcinomas . In determining the utilised dose of Cetrorelix, we selected the pharmacologic dose of 10 À5 M based on literature reports for Cetrorelix (Tang et al, 2002) and a related LHRH analogue goserelin (Dondi et al, 1994;Jungwirth et al, 1997a, b;Limonta et al, 1998;Wells et al, 2002). In addition, growth studies from our laboratory utilising Cetrorelix at 10 À5 M inhibited DU-145 WT proliferation without causing cell death (data not shown).…”
Section: Resultsmentioning
confidence: 99%
“…The clinical application of GnRH analogues in the treatment of hormone-dependent malignancies is primarily based on their ability to inhibit the hypophysealÁ/gonadal axis through the desensitization of gonadotropes and hence the suppression of circulating levels of sex steroids [21,22]. In addition, specific membrane receptors for GnRH, at least type I, have been found in a high percentage of human prostate tumours and various rat and human PC cell lines [1,2,4,10,16,17]. These receptors mediate inhibiting effects of GnRH analogues in vitro suggesting that direct inhibitory effects on the tumour may be of importance also in vivo.…”
Section: Discussionmentioning
confidence: 99%
“…Evidence is now accumulating that GnRH analogues may inhibit tumour growth, not only by suppressing the pituitary Á/testicular axis but also by acting directly at the level of the tumour [1,2]. Specific binding sites for GnRH (GnRH-R type I and II) have been characterized in a number of extrapituitary tissues including the prostate [3 Á/5].…”
Section: Introductionmentioning
confidence: 99%
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