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1.

001-es BibID:BIBFORM099555
Első szerző:Cai, Ren-Zhi
Cím:Synthesis of potent antagonists of receptors for growth hormone-releasing hormone with antitumor and anti-inflammatory activity / Renzhi Cai, Xianyang Zhang, Haibo Wang, Tengjiao Cui, Gabor Halmos, Wei Sha, Jinlin He, Petra Popovics, Irving Vidaurre, Chongxu Zhang, Mehdi Mirsaeidi, Andrew V. Schally
Dátum:2022
ISSN:0196-9781
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Peptides. - 150 (2022), p. 1-13. -
További szerzők:Zhang, Xianyang Wang, Haibo Cui, Tengjiao Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Sha, Wei He, Jinlin Popovics Petra Vidaurre, Irving Zhang, Chongxu Mirsaeidi, Mehdi Schally, Andrew Victor
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DOI
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2.

001-es BibID:BIBFORM011626
Első szerző:Hohla, Florian
Cím:GHRH antagonist causes DNA damage leading to p21 mediated cell cycle arrest and apoptosis in human colon cancer cells / Florian Hohla, Stefan Buchholz, Andrew V. Schally, Stefan Seitz, Ferenc G. Rick, Luca Szalontay, Jozsef L. Varga, Marta Zarandi, Gabor Halmos, Irving Vidaurre, Awtar Krishan, Metin Kurtoglu, Sudhir Chandna, Elmar Aigner, Christian Datz
Dátum:2009
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cell Cycle. - 8 : 19 (2009), p. 3149-3156. -
További szerzők:Buchholz, Stefan Schally, Andrew Victor Seitz, Stephan Rick Ferenc G. Szalontay Luca Varga József L. Zarándi Márta Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Vidaurre, Irving Krishan, Awtar Kurtoglu, Metin Chandna, Sudhir Aigner, Elmar Datz, Christian
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3.

001-es BibID:BIBFORM030454
Első szerző:Klukovits Anna
Cím:Novel antagonists of growth hormone-releasing hormone inhibit growth and vascularization of human experimental ovarian cancers / Anna Klukovits, Andrew V. Schally, Luca Szalontay, Irving Vidaurre, Andrea Papadia, Marta Zarandi, Jozsef L. Varga, Norman L. Block, Gabor Halmos
Dátum:2012
ISSN:0008-543X
Megjegyzések:Antagonists of growth hormone-releasing hormone (GHRH) inhibit the proliferation of various human cancer cell lines and experimental tumors by mechanisms that include direct action on GHRH receptors in cancer cells. METHODS: In this study, the effects of newly synthesized GHRH antagonists, MIA-313, MIA-602, MIA-604, and MIA-610, were investigated in 2 human ovarian epithelial adenocarcinoma cell lines, OVCAR-3 and SKOV-3, in vitro and in vivo. The expression of receptors for GHRH was demonstrated by Western blot analysis and ligand competition methods in the OVCAR-3 and SKOV-3 cell lines and in tumors from those cells grown in athymic nude mice. The effects of GHRH antagonists on the secretion of vascular endothelial growth factor (VEGF) by OVCAR-3 cells and on the vascularization of OVCAR-3 xenografts also were evaluated. RESULTS: Both the pituitary and the splice variant type 1 (SV1) GHRH receptors were detected in the 2 cell lines and in tumor xenografts, and SV1 was expressed at higher levels. Cell viability assays revealed the antiproliferative effect of all GHRH antagonists that were. Maximal tumor growth inhibition was approximately 75% in both models. MIA-313 and MIA-602 decreased VEGF secretion of OVCAR-3 cells, as measured by enzyme-linked immunosorbent assay, and reduced tumor vascularization in a Matrigel plug assay, but caused no change in the expression of VEGF or VEGF receptor in the terminal ileum of mice with OVCAR-3 tumors. CONCLUSIONS: Results from the current study indicated that a he novel approach based on GHRH antagonists may offer more effective therapeutic alternatives for patients with advanced ovarian cancer and who do not tolerate conventional anti-VEGF therapy.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Molekulatudomány
Megjelenés:Cancer. - 118 : 3 (2012), p. 670-680. -
További szerzők:Schally, Andrew Victor Szalontay Luca Vidaurre, Irving Papadia, Andrea Zarándi Márta Varga József L. Block, Norman L. Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Peptid hormon és növekedési faktor receptorok mint molekuláris célpontok a humán rosszindulatú daganatok diagnosztikájában és terápiájában
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4.

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
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5.

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
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6.

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
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7.

001-es BibID:BIBFORM047176
035-os BibID:PMID:23744510
Első szerző:Szepesházi Károly
Cím:Powerful Inhibition of Experimental Human Pancreatic Cancers by Receptor Targeted Cytotoxic LH-RH analog AEZS-108 / Karoly Szepeshazi, Andrew V. Schally, Norman L. Block, Gabor Halmos, Mehrdad Nadji, Luca Szalontay, Irving Vidaurre, Andrew Abi-Chaker, Ferenc G. Rick
Dátum:2013
Megjegyzések:Pancreatic carcinoma is one of the cancers with the worse prognosis, thus any therapeutic improvement is imperative. Cytotoxic LH-RH analog, AN-152 (proprietary designation, AEZS-108), consisting of doxorubicin (DOX) conjugated to D-Lys6LH-RH, is now in clinical trials for targeted therapy of several sex hormone-dependent tumors that express LH-RH receptors. We investigated LH-RH receptors in human pancreatic carcinoma and the effects of AN-152 (AEZS-108) on experimental pancreatic cancers. We determined LH-RH receptor presence in human pancreatic cancer samples by immunohistochemistry and, in three human pancreatic cancer lines (SW-1990, Panc-1 and CFPAC-1), by binding assays and Western blotting. The effects of the cytotoxic LH-RH analog were investigated on growth of these same cancer lines xenografted into nude mice. We also analyzed differences between the antitumor effects of the cytotoxic analog and its cytotoxic radical alone, doxorubicin (DOX), on the expression of cancer-related genes by PCR arrays. LH-RH receptors were expressed in two randomly selected surgically removed human pancreatic cancer samples and in all three cancer lines. Cytotoxic LH-RH analogs powerfully inhibited growth of all three tumor lines in nude mice; AN-152 was significantly stronger than DOX on Panc-1 and CFPAC-1 cancers. PCR array showed that cytotoxic LH-RH analog AN-152 affected the expression of genes associated with cellular migration, invasion, metastasis and angiogenesis more favorably than DOX, however the changes in gene expression varied considerably among the three cancer lines. Cytotoxic LH-RH analog, AEZS-108, may be a useful agent for the treatment of LH-RH receptor positive advanced pancreatic carcinoma.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekulatudomány
Megjelenés:Oncotarget (electronic resources). - 4 : 5 (2013), p. 751-760. -
További szerzők:Schally, Andrew Victor Block, Norman L. Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Nadji, Mehrdad Szalontay Luca Vidaurre, Irving Abi-Chaker, Andrew Rick Ferenc G.
Pályázati támogatás:K81596
OTKA
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Peptid hormon és növekedési faktor receptorok mint molekuláris célpontok a humán rosszindulatú daganatok diagnosztikájában és terápiájában
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8.

001-es BibID:BIBFORM037000
Első szerző:Szepesházi Károly
Cím:Powerful inhibition of in-vivo growth of experimental hepatic cancers by bombesin/gastrin-releasing peptide antagonist RC-3940-II / Szepeshazi Karoly, Schally Andrew V., Rick Ferenc G., Block Norman L., Vidaurre Irving, Halmos Gabor, Szalontay Luca
Dátum:2012
ISSN:0959-4973
Megjegyzések:Hepatic carcinoma is a major health problem worldwide. Its incidence is increasing in Western countries and there is currently no effective systemic therapy against it. Targeted treatment modalities developed in the past few years have provided very limited success. Development of new treatment strategies is therefore essential. We investigated the effects of bombesin/gastrin-releasing peptide (BN/GRP) antagonist RC-3940-II on experimental human liver cancers in nude mice. SK-Hep-1 and Hep-G2 cancers transplanted subcutaneously into nude mice were treated daily with 10 or 20 mikrog of RC-3940-II. Tumor growth was monitored for 50-184 days in five experiments. Tumor gene expression was analyzed with PCR array and protein expression by immunoblotting. Characteristics of BN/GRP receptors in the tumors were analyzed by binding assays. Effects of RC-3940-II on cell proliferation were investigated in vitro. RC-3940-II inhibited the growth of SK-Hep-1 cancers in nude mice by 65-98%, with total regression in 9 of 36 tumors in three experiments. The BN/GRP antagonist inhibited the growth of Hep-G2 cancers as well by 73-82% in two experiments, being effective even on originally large tumors. Gene expression analysis showed an increase in several angiogenesis inhibitors and decrease in proangiogenic genes after RC-3940-II treatment. Receptor assays demonstrated high-affinity binding sites for BN/GRP in both tumor lines. BN/GRP antagonist RC-3940-II powerfully inhibits growth of SK-Hep-1 and Hep-G2 cancers in nude mice. Its effect may be linked to changes in expression of those cancer genes important in angiogenesis, invasion, and metastasis. RC-3940-II may be considered for further investigations in treatment of liver cancers.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekulatudomány
Megjelenés:Anti-Cancer Drugs. - 23 : 9 (2012), p. 906-913. -
További szerzők:Schally, Andrew Victor Rick Ferenc G. Block, Norman L. Vidaurre, Irving Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Szalontay Luca
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Peptid hormon és növekedési faktor receptorok mint molekuláris célpontok a humán rosszindulatú daganatok diagnosztikájában és terápiájában
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM036738
035-os BibID:PMID:22824624
Első szerző:Szepesházi Károly
Cím:Receptor-targeted therapy of human experimental urinary bladder cancers with cytotoxic LH-RH analog AN-152 [AEZS- 108] / Karoly Szepeshazi, Andrew V. Schally, Gunhild Keller, Norman L. Block, Daniel Benten, Gabor Halmos, Luca Szalontay, Irving Vidaurre, Miklos Jaszberenyi, Ferenc G. Rick
Dátum:2012
Megjegyzések:Many bladder cancers progress to invasion with poor prognosis; new therapeutic methods are needed. We developed a cytotoxic LH-RH analog, AN-152 (AEZS-108) containing doxorubicin (DOX), for targeted therapy of cancers expressing LHRH receptors. We investigated the expression of LH-RH receptors in clinical bladder cancers and in HT-1376, J82, RT-4 and HT-1197 human bladder cancer lines. The effect of analog, AN-152, on growth of these tumor lines xenografted into nude mice was analyzed. Using molecular and functional assays, we also evaluated the differences between the effects of AN-152, and DOX alone. We demonstrated the expression of LH-RH receptors on 18 clinical bladder cancers by immunohistochemistry and on four human urinary bladder cancer lines HT-1376, J82, RT-4 and HT-1197 by Western blotting and binding assays. AN-152 powerfully inhibited growth of these bladder cancers in nude mice. AN-152 exerted greater effects than DOX and was less toxic. DOX activated strong multidrug resistance mechanisms in RT-4 and HT-1197 cancers, while AN-152 had no or less such effect. PCR assays and in vitro studies revealed differences in the action of AN-152 and DOX on the expression of genes involved in apoptosis. These results suggest that targeted cytotoxic LH-RH analog, AN-152 (AEZS- 108), should be examined for treatment of patients with LH-RH receptor positive invasive bladder cancers.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekulatudomány
külföldön készült közlemény
Megjelenés:Oncortarget (electronic resources). - 3 : 7 (2012), p. 686-699. -
További szerzők:Schally, Andrew Victor Keller, Gunhild Block, Norman L. Benten, Daniel Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Szalontay Luca Vidaurre, Irving Jászberényi Miklós Rick Ferenc G.
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Peptid hormon és növekedési faktor receptorok mint molekuláris célpontok a humán rosszindulatú daganatok diagnosztikájában és terápiájában
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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