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1.

001-es BibID:BIBFORM049347
Első szerző:Cai, Ren-Zhi
Cím:Synthesis of new potent agonistic analogs of growth hormone-releasing hormone (GHRH) and evaluation of their endocrine and cardiac activities / Renzhi Cai, Andrew V. Schally, Tengjiao Cui, Luca Szalontay, Gabor Halmos, Wei Sha, Magdolna Kovacs, Miklos Jaszberenyi, Jinlin He, Ferenc G. Rick, Petra Popovics, Rosemeire Kanashiro-Takeuchi, Joshua M. Hare, Norman L. Block, Marta Zarandi
Dátum:2013
ISSN:0196-9781
Megjegyzések:AbstractIn view of the recent findings of stimulatory effects of GHRH analogs, JI-34, JI-36 and JI-38, on cardiomyocytes, pancreatic islets and wound healing, three series of new analogs of GHRH(1-29) have been synthesized and evaluated biologically in an endeavor to produce more potent compounds. "Agmatine analogs", MR-356 (N-Me-Tyr1-JI-38), MR-361(N-Me-Tyr1, D-Ala2-JI-38) and MR-367(N-Me-Tyr1, D-Ala2, Asn8-JI-38), in which Dat in JI-38 is replaced by N-Me-Tyr1, showed improved relative potencies on GH release upon subcutaneous administration in vivo and binding in vitro. Modification with N-Me-Tyr1 and Arg29-NHCH3 as in MR-403 (N-Me-Tyr1, D-Ala2, Arg29-NHCH3-JI-38), MR-406 (N-Me-Tyr1, Arg29-NHCH3-JI-38) and MR-409 (N-Me-Tyr1, D-Ala2, Asn8, Arg29-NHCH3-JI-38), and MR-410 (N-Me-Tyr1, D-Ala2, Thr8, Arg29-NHCH3-JI-38) resulted in dramatically increased endocrine activities. These appear to be the most potent GHRH agonistic analogs so far developed. Analogs with Apa30-NH2 such as MR-326 (N-Me-Tyr1, D-Ala2, Arg29, Apa30-NH2-JI-38), and with Gab30-NH2, as MR-502 (D-Ala2, 5F-Phe6, Ser28, Arg29,Gab30-NH2-JI-38) also exhibited much higher potency than JI-38 upon i.v. administration. The relationship between the GH-releasing potency and the analog structure is discussed. Fourteen GHRH agonists with the highest endocrine potencies were subjected to cardiologic tests. MR-409 and MR-356 exhibited higher potency than JI-38 in activating myocardial repair in rats with induced myocardial infarction. As the previous class of analogs, exemplified by JI-38, had shown promising results in multiple fields including cardiology, diabetes and wound healing, our new, more potent, GHRH agonists should manifest additional efficacy for possible medical applications.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
5-aminopentanoyl
Abu
Agm
Apa
Cardioprotection
Dat
EF
Fpa5
GH
GH-releasing hormone
GHRH
Gab
IGF
MI
MeCN
N-Me-Tyr
N-methyl-tyrosine
PKA
PKC
PLC
TOF
acetonitrile
agmatine
des-amino-tyrosine
ejection fraction
gamma-amino-butanoyl
growth hormone
hGHRH agonist
hGHRH(1-29)
human
i.v.
insulin-like growth factor
intravenous, myocardial infarction
pentafluoro-Phe, phospholipase C
protein kinase A
protein kinase C
s.c.
s.c. administration
subcutaneous
time-of-flight
Megjelenés:Peptides. - 52C (2013), p. 104-112. -
További szerzők:Schally, Andrew Victor Cui, Tengjiao Szalontay Luca Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Sha, Wei Kovács Magdolna Jászberényi Miklós He, Jinlin Rick Ferenc G. Popovics Petra Kanashiro-Takeuchi, Rosemeire Hare, Joshua M. Block, Norman L. Zarándi Márta
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0025
TÁMOP
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2.

001-es BibID:BIBFORM004056
Első szerző:Heinrich, Elmar
Cím:Dose-dependent growth inhibition in vivo of PC-3 prostate cancer with a reduction in tumoral growth factors after therapy with GHRH antagonist MZ-J-7-138 / Elmar Heinrich, Andrew V. Schally, Stefan Buchholz, Ferenc G. Rick, Halmos Gábor, Mile Melinda, Kate Groot, Florian Hohla, Zarandi Márta, Jozsef L. Varga
Dátum:2008
Megjegyzések:Antagonists of growth hormone-releasing hormone (GHRH) inhibit the growth of various cancers and affect tumoral growth factors. Methods: We investigated the effect of a new GHRH antagonist MZ-J-7-138 at doses of 1.25, 2.5, 5 and 10 mű g/day s.c. on the growth of PC-3 human androgen independent prostate cancers xenografted s.c. into nude mice. Binding assays were used to investigate GHRH receptors. The levels of IGF-II and VEGF in tumors were measured by radioimmunoassays. Results: Treatment with 2.5, 5, and 10 mű g/day MZ-J-7-138 caused a significant dose-dependent growth reduction of PC-3 tumors. The greatest inhibition of 78% was obtained with 10 mű g/day. The suppression of IGF-II protein levels in tumors was seen at all doses of MZ-J-7-138, but only 10 microg dose induced a significant inhibition. MZ-J-7-138 also reduced VEGF protein levels, the inhibition being significant at doses of 5 and 10 microg. Specific high affinity binding sites for GHRH were found on PC-3 tumors using 125I-labeled GHRH antagonist JV-1-42. MZ-J-7-138 displaced radiolabeled JV-1-42 with an IC50 of 0.32 nM indicating its high affinity to GHRH receptors. Real-time PCR analyses detected splice variant 1 (SV1) of GHRH receptor (GHRH-R) as well as pituitary type of GHRH-R and GHRH ligand. Conclusion: Our results demonstrate the efficacy of GHRH antagonist MZ-J-7-138 in suppressing growth of PC-3 prostate cancer at doses lower than previous antagonists. The reduction of levels of growth factors such as VEGF and IGF-II in tumors by GHRH antagonist was correlated with the suppression of tumor growth.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Prostate. - 68 : 16 (2008), p. 1763-1772. -
További szerzők:Schally, Andrew Victor Buchholz, Stefan Rick Ferenc G. Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Mile Melinda (1983-) (gyógyszerész) Groot, Kate Hohla, Florian Zarándi Márta Varga József L.
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3.

001-es BibID:BIBFORM033538
035-os BibID:WOS:000240968100047
Első szerző:Hohla, Florian
Cím:Synergistic inhibition of growth of lung carcinomas by antagonists of growth hormone-releasing hormone in combination with docetaxel / Florian Hohla, Andrew V. Schally, Karoly Szepeshazi, Jozsef L. Varga, Stefan Buchholz, Frank Köster, Elmar Heinrich, Gabor Halmos, Ferenc G. Rick, Chandrika Kannadka, Christian Datz, Celia A. Kanashiro
Dátum:2006
ISSN:0027-8424
Megjegyzések:We investigated the effect of antagonists of growth hormone-releasing hormone (GHRH) MZ-J-7-138 and JV-1-92 on H460 human non-small cell lung carcinoma (NSCLC) xenografted orthotopically into nude mice. Treatment with MZ-J-7-138 or JV-1-92 inhibited orthotopic growth of H460 NSCLC by 52-65% (P < 0.001) and was associated with a significant decrease in protein expression of K-Ras, cyclooxygenase-2 (Cox-2) and phospho-Akt (pAkt). in other experiments, treatment with MZ-J-7-138 or docetaxel reduced tumor volume of s.c. xenografted H460 human NSCLC by 30-36% (P < 0.01). The combination of MZ-J-7-138 and docetaxel resulted in a synergistic growth inhibition of H460 NSCLC xenografts of 63%. MZ-J-7-138 alone or in combination with docetaxel significantly reduced protein levels of K-Ras, Cox-2, and pAkt by 56-63%. Docetaxel given singly diminished the protein levels only of Cox-2 and did not affect K-Ras and pAkt. High-affinity binding sites, mRNA, and protein expression of pituitary GHRH receptors and its splice variant (SV) 1 were found in H460. H460 NSCLC cells contained GHRH peptide, and its growth was significantly inhibited in vitro by 10 mu M MZ-J-7-138 (P < 0.001). Serum insulin-like growth factor 1 (IGF1) was not reduced by either GHRH antagonists. These findings suggest that antiproliferative effects of GHRH antagonists in H460 NSCLC are associated with down-regulation of K-Ras, Cox-2, and pAkt. In conclusion, GHRH antagonists in combination with docetaxel synergistically inhibit growth of H460 NSCLC and the expression of K-ras, Cox-2, and pAkt, which might abrogate the signal transduction pathways for cell growth stimulation and therapeutic resistance.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Proceedings of The National Academy of Sciences of The United States of America. - 103 : 39 (2006), p. 14513-14518. -
További szerzők:Schally, Andrew Victor Szepesházi Károly Varga József L. Buchholz, Stefan Köster, Frank Heinrich, Elmar Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Rick Ferenc G. Kannadka, Chandrika Datz, Christian Kanashiro, Celia A.
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4.

001-es BibID:BIBFORM019785
Első szerző:Hohla, Florian
Cím:Targeted cytotoxic somatostatin analog AN-162 inhibits growth of human colon carcinomas and increases sensitivity of doxorubicin resistant murine leukemia cells / Hohla Florian, Buchholz Stefan, Schally Andrew V., Krishan Awtar, Rick Ferenc G., Szalontay Luca, Papadia Andrea, Halmos Gabor, Koster Frank, Aigner Elmar, Datz Christian, Seitz Stephan
Dátum:2010
ISSN:0304-3835
Megjegyzések:The effect of the targeted cytotoxic somatostatin (SST) analog AN-162, consisting of doxorubicin (DOX) conjugated to SST carrier RC-121, was investigated on the growth of human colorectal cancer (CRC) cell lines HT-29, HCT-15, and HCT-116 and a DOX-resistant mouse leukemia cell line P388/R84. mRNA for SST-receptors and high affinity binding sites for SST were detected in all CRC cell lines and in P388/R84 cells. In contrast to DOX alone, AN-162 blocked HCT-116 cells and P388/R84 cells in S/G2 phase and increased the number of apoptotic cells. In vivo, AN-162 reduced the volume of CRC xenografts more effectively than its unconjugated components. Our results suggest that AN-162 inhibits growth of experimental CRC more effectively than DOX and increases sensitivity of DOX resistant human leukemia cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cancer Letters. - 294 : 1 (2010), p. 35-42. -
További szerzők:Buchholz, Stefan Schally, Andrew Victor Krishan, Awtar Rick Ferenc G. Szalontay Luca Papadia, Andrea Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Koster, Frank Aigner, Elmar Datz, Christian Seitz, Stephan
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5.

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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6.

001-es BibID:BIBFORM040825
Első szerző:Papadia, Andrea
Cím:Growth Hormone-Releasing Hormone Antagonists Inhibit Growth of Human Ovarian Cancer / Papadia, A., Schally, A., Halmos, G., Varga, J., Seitz, S., Buchholz, S., Rick, F., Zarandi, M., Bellyei, S., Treszl, A., Szalontay, L., Lucci, J. A.
Dátum:2011
ISSN:0018-5043
Megjegyzések:Epithelial ovarian carcinoma is the leading cause of cancer-related deaths among women with gynecologic malignancies. Antagonists of the growth hormone-releasing hormone (GHRH) have been shown to inhibit growth of various cancers through endocrine, autocrine, and paracrine mechanisms. In this study, we have investigated the effects of GHRH antagonists (GHRHa) in ES-2 human clear cell ovarian cancer and in UCI-107 human serous ovarian cancer in vitro and in vivo. We evaluated the expression of mRNA for GHRH receptor, the binding to GHRH receptors, in specimens of ES-2 ovarian cancer. We evaluated also the in vitro effects of GHRHa on ES-2 cells and the in vivo effect of 2 different GHRHa on ES-2 and UCI-107 tumors. Nude mice bearing xenografts on ES-2 and UCI-107 ovarian cancer were treated with JMR-132 and MZ-J-7-118, respectively. Tumor growth was compared to control. ES-2 cells expressed mRNA for the functional splice variant SV1 of the GHRH receptor. JMR-132 inhibited cell proliferation in vitro by 42% and 18% at 10 and 1 gammaM concentration, respectively. Specific high affinity receptors for GHRH were detected in ES-2 cancer samples. In vivo daily subcutaneous injections of GHRHa significantly reduced tumor growth compared to a control group in both animal models. Our results indicate that GHRHa such as JMR-132 and MZ-J-7-118 can inhibit the growth of human ovarian cancer. The efficacy of GHRHa in ovarian cancer should be assessed in clinical trials.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Hormone And Metabolic Research. - 43 : 11 (2011), p. 816-820. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Varga J. (orvos) Seitz, S. Buchholz, Stefan Rick Ferenc G. Zarándi Márta Bellyei Szabolcs Treszl Andrea (1974-) (molekuláris biológus) Szalontay Luca Lucci III, J. A.
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7.

001-es BibID:BIBFORM015979
Első szerző:Papadia, Andrea
Cím:Experimental therapy of ES-2 human platinum resistant ovarian cancer with growth hormone-releasing hormone antagonist JMR-132 or with targeted cytotoxic analog somatostatin AN-162 / A. Papadia, A. Schally, S. Seitz, S. Buchholz, F. Rick, L. Szalontay, G. Halmos, A. Treszl, J. A. Lucci
Dátum:2004
ISSN:0090-8258
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Megjelenés:Gynecologic Oncology. - 112 : 2 (2004), p. S128-S129. -
További szerzők:Schally, Andrew Victor Seitz, Stephan Buchholz, Stefan Rick Ferenc G. Szalontay Luca Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Treszl Andrea (1974-) (molekuláris biológus) Lucci III, J. A.
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8.

001-es BibID:BIBFORM019787
Első szerző:Pozsgai E.
Cím:The inhibitory effect of a novel cytotoxic somatostatin analogue AN-162 on experimental glioblastoma / Pozsgai, E., Schally, A. V., Halmos, G., Rick, F., Bellyei, S.
Dátum:2010
ISSN:0018-5043
Megjegyzések:Glioblastoma multiforme is the most common and most aggressive type of high grade tumor with a poor prognosis upon discovery. Based on earlier promising results earned with AN-162, a doxorubicin molecule linked to somatostatin (SST) analogue RC-160, it was our aim to determine the effect of AN-162 on DBTRG-05 glioblastoma cell line, and to test its efficacy in experimental brain tumors. We detected the expression of mRNA for somatostatin receptor (SSTR) subtypes 2 and 3 in DBTRG-05 cells with RT-PCR. Using ligand competition assay, specific high affinity receptors for somatostatin were found. The MTT assay showed that both AN-162 and doxorubicin (DOX) significantly inhibited cell proliferation and that there was no significant difference between the effects in vitro. Nude mice were xenografted with DBTRG-05 glioblastoma tumors. AN-162 showed a significant inhibition of tumor growth compared with the control group and the groups treated with equimolar doses of doxorubicin, somatostatin analogue RC-160, or the unconjugated mixture of doxorubicin plus RC-160. The tumor doubling time in the group of animals treated with AN-162 was extended and was significantly different from doubling times in the control group and in the other treatment groups. Our study clearly demonstrates a potent inhibitory effect of AN-162 in experimental glioblastoma, thus suggesting the possibility of its utilization in patients suffering from malignant brain cancer.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Hormone And Metabolic Research. - 42 : 11 (2010), p. 781-786. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Rick Ferenc G. Bellyei Szabolcs
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9.

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
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10.

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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11.

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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12.

001-es BibID:BIBFORM011473
Első szerző:Seitz, Stephan
Cím:Preclinical evaluation of properties of a new targeted cytotoxic somatostatin analog, AN-162 (AEZS-124), and its effects on tumor growth inhibition / Seitz S., Schally A. V., Treszl A., Papadia A., Rick F., Szalontay L., Szepeshazi K., Ortmann O., Halmos G., Hohla F., Buchholz S.
Dátum:2009
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Anti-Cancer Drugs. - 20 : 7 (2009), p. 553-558. -
További szerzők:Schally, Andrew Victor Treszl Andrea (1974-) (molekuláris biológus) Papadia, Andrea Rick Ferenc G. Szalontay Luca Szepesházi Károly Ortmann, Olaf Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Hohla, Florian Buchholz, Stefan
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