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001-es BibID:	BIBFORM041791
Első szerző:	Rick Ferenc G.
Cím:	Shrinkage of experimental benign prostatic hyperplasia and reduction of prostatic cell volume by a gastrin-releasing peptide antagonist / Rick F. G., Abi-Chaker A., Szalontay L., Perez R., Jaszberenyi M., Jayakumar A. R., Shamaladevi N., Szepeshazi K., Vidaurre I., Halmos G., Krishan A., Block N. L., Schally A. V.
Dátum:	2013
Megjegyzések:	Gastrin releasing-peptide (GRP) is a potent growth factor in many malignancies. Benign prostatic hyperplasia (BPH) is a progressive age-related proliferation of glandular and stromal tissues; various growth factors and inflammatory processes are involved in its pathogenesis. We have demonstrated that potent antagonists of GRP inhibit growth of experimental human tumors including prostate cancer, but their effect on models of BPH has not been studied. Here, we evaluated the effects of GRP antagonist RC-3940-II on viability and cell volume of BPH-1 human prostate epithelial cells and WPMY-1 prostate stromal cells in vitro, and in testosterone-induced BPH in Wistar rats in vivo. RC-3940-II inhibited the proliferation of BPH-1 and WPMY-1 cells in a dose-dependent manner and reduced prostatic cell volume in vitro. Shrinkage of prostates was observed after 6 wk of treatment with RC-3940-II: a 15.9% decline with 25 ?g/d; and a 18.4% reduction with 50 ?g/d (P < 0.05 for all). Significant reduction in levels of proliferating cell nuclear antigen, NF-??/p50, cyclooxygenase-2, and androgen receptor was also seen. Analysis of transcript levels of genes related to growth, inflammatory processes, and signal transduction showed significant changes in the expression of more than 90 genes (P < 0.05). In conclusion, GRP antagonists reduce volume of human prostatic cells and lower prostate weight in experimental BPH through direct inhibitory effects on prostatic GRP receptors. GRP antagonists should be considered for further development as therapy for BPH.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Proceedings of the National Academy of Sciences of the United States of America. - 110 : 7 (2013), p. 2617-2622. -
További szerzők:	Abi-Chaker, Andrew Szalontay Luca Perez, Roberto Jászberényi Miklós Jayakumar, Arumugam R. Shamaladevi, Nagarajarao Szepesházi Károly Vidaurre, Irving Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Krishan, Awtar Block, Norman L. Schally, Andrew Victor
Pályázati támogatás:	TÁMOP-4.2.2.A-11/1/KONV-2012-0025 TÁMOP
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM033533
035-os BibID:	WOS:000287844400058
Első szerző:	Rick Ferenc G.
Cím:	Antagonists of growth hormone-releasing hormone (GHRH) reduce prostate size in experimental benign prostatic hyperplasia / Ferenc G. Rick, Andrew V. Schally, Norman L. Block, Mehrdad Nadji, Karoly Szepeshazi, Marta Zarandi, Irving Vidaurre, Roberto Perez, Gabor Halmos, Luca Szalontay
Dátum:	2011
ISSN:	0027-8424
Megjegyzések:	Growth hormone-releasing hormone (GHRH), a hypothalamic polypeptide, acts as a potent autocrine/paracrine growth factor in many cancers. Benign prostatic hyperplasia (BPH) is a pathologic proliferation of prostatic glandular and stromal tissues; a variety of growth factors and inflammatory processes are inculpated in its pathogenesis. Previously we showed that potent synthetic antagonists of GHRH strongly inhibit the growth of diverse experimental human tumors including prostate cancer by suppressing various tumoral growth factors. The influence of GHRH antagonists on animal models of BPH has not been investigated. We evaluated the effects of the GHRH antagonists JMR-132 given at doses of 40 mu g/d, MIA-313 at 20 mu g/d, and MIA-459 at 20 mu g/d in testosterone-induced BPH in Wistar rats. Reduction of prostate weights was observed after 6 wk of treatment with GHRH antagonists: a 17.8% decrease with JMR-132 treatment; a 17.0% decline with MIA-313 treatment; and a 21.4% reduction with MIA-459 treatment (P < 0.05 for all). We quantified transcript levels of genes related to growth factors, inflammatory cytokines, and signal transduction and identified significant changes in the expression of more than 80 genes (P < 0.05). Significant reductions in protein levels of IL-1 beta, NF-kappa beta/p65, and cyclooxygenase-2 (COX-2) also were observed after treatment with a GHRH antagonist. We conclude that GHRH antagonists can lower prostate weight in experimental BPH. This reduction is caused by the direct inhibitory effects of GHRH antagonists exerted through prostatic GHRH receptors. This study sheds light on the mechanism of action of GHRH antagonists in BPH and suggests that GHRH antagonists should be considered for further development as therapy for BPH.
Tárgyszavak:	Orvostudományok Sporttudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Proceedings of The National Academy of Sciences of The United States of America. - 108 : 9 (2011), p. 3755-3760. -
További szerzők:	Schally, Andrew Victor Block, Norman L. Nadji, Mehrdad Szepesházi Károly Zarándi Márta Vidaurre, Irving Perez, Roberto Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Szalontay Luca
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM019788
Első szerző:	Rick Ferenc G.
Cím:	LHRH antagonist Cetrorelix reduces prostate size and gene expression of proinflammatory cytokines and growth factors in a rat model of benign prostatic hyperplasia / Rick Ferenc G., Schally Andrew V., Block Norman L., Halmos Gabor, Perez Roberto, Fernandez Jesus B., Vidaurre Irving, Szalontay Luca
Dátum:	2011
ISSN:	0270-4137
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	The Prostate. - 71 : 7 (2011), p. 736-747. -
További szerzők:	Schally, Andrew Victor Block, Norman L. Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Perez, Roberto Fernandez, Jesus B. Vidaurre, Irving Szalontay Luca
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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