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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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2.

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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3.

001-es BibID:BIBFORM033689
035-os BibID:PMID:9254895 WOS:A1997XN99200002
Első szerző:Jungwirth, Andreas
Cím:Luteinizing hormone-releasing hormone antagonist Cetrorelix (SB-75) and bombesin antagonist RC-3940-II inhibit the growth of androgen-independent PC-3 prostate cancer in nude mice / Andreas Jungwirth, Georg Galvan, Jacek Pinski, Gabor Halmos, Karoly Szepeshazi, Ren-Zhi Cai, Kate Groot, Andrew V. Schally
Dátum:1997
ISSN:0270-4137
Megjegyzések:BACKGROUND: Hormones like bombesin (BN)/gastrin-releasing peptide (GRP) and luteinizing hormone-releasing hormone (LH-RH) and growth factors such as epidermal growth factor (EGF) might be involved in the relapse of prostate cancer under androgen ablation therapy. Interference with receptors for BN/GRP, LH-RH, or EGF might provide a therapeutic approach to inhibit tumor growth of androgen-independent prostate cancer. METHODS: LH-RH antagonist Cetrorelix (SB-75) and the BN/GRP antagonist RC-3940-II were tested for their effects on the growth of the androgen-independent PC-3 human prostate cancer cell line xenografted into nude mice. Tumor growth, serum hormone levels, and receptor concentrations for BN/GRP and EGF were measured. RESULTS: When the treatment was started, tumor volume in all groups was 70-80 mm3. After 4 weeks, tumor volume in the control animals injected with saline was 871 +/- 233 mm3 and that of animals treated with Cetrorelix only 197 +/- 61 mm3. The BN/GRP antagonist RC-3940-II also significantly reduced PC-3 tumor volume in nude mice to 122 +/- 20 mm3. The combination of Cetrorelix and RC-3940-II produced no additional inhibition. High-affinity receptors for EGF were detected in the tumor membranes and their number was significantly decreased after administration of Cetrorelix or RC-3940-II. CONCLUSIONS: These findings demonstrate that LH-RH antagonists and BN/GRP antagonists inhibit the growth of the androgen-independent prostate cancer cell line PC-3 in vivo. Both analogs may exert a direct inhibitory effect on tumor growth through a down-regulation of EGF receptors.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Prostate. - 32 : 3 (1997), p. 164-172. -
További szerzők:Galvan, Georg Pinski, Jacek Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Szepesházi Károly Cai, Ren-Zhi Groot, Kate Schally, Andrew Victor
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4.

001-es BibID:BIBFORM033687
035-os BibID:WOS:A1997XJ25000027
Első szerző:Jungwirth, Andreas
Cím:Inhibition of growth of androgen-independent DU-145 prostate cancer in vivo by luteinising hormone-releasing hormone antagonist Cetrorelix and bombesin antagonists RC-3940-II and RC-3950-II / A. Jungwirth, J. Pinski, G. Galvan, G. Halmos, K. Szepeshazi, R. Z. Cai, K. Groot, M. Vadillo-Buenfil, A. V. Schally
Dátum:1997
ISSN:0959-8049
Megjegyzések:The aim of this study was to test the antagonist of LH-RH (Cetrorelix), agonist [D-Trp6]LH-RH (triptorelin) and new bombesin antagonists RC-3940-II and RC-3950-II for their effect on the growth of an androgen-independent prostate cancer cell line, DU-145, xenografted into nude mice. Xenografts were grown in male nude mice, and after 4 weeks, the animals were treated either with saline (control) or with one of the analogues. One group of mice was given a combination of Cetrorelix and RC-3950-II. Treatment was given for 4 weeks. Tumour and body weights, and tumour volumes were measured. At sacrifice, tumours were dissected for histological examination and receptor studies. Serum was collected for measurement of hormone levels. The final tumour volume in control animals injected with saline was 577 +/- 155 mm3 and that of animals treated with Cetrorelix only 121.4 +/- 45 mm3 (P < 0.01). Bombesin antagonists RC-3940-II and RC-3950-II also significantly reduced DU-145 tumour volume in nude mice to 84.9 +/- 19.9 and 96.8 +/- 28 mm3, respectively. Agonist [D-Trp6]LH-RH did not significantly inhibit tumour growth. Serum levels of LH were decreased to 0.08 +/- 0.02 ng/ml (P < 0.05) in the Cetrorelix treated group as compared to 1.02 +/- 0.1 ng/ml for the controls, and testosterone levels were reduced to castration levels (0.01 +/- 0.01 ng/ml). Specific receptors for EGF and LH-RH in DU-145 tumours were significantly downregulated after treatment with Cetrorelix, RC-3940-II and RC-3950-II. Although LH-RH could be a local regulator of growth of prostate cancer, the fall in LH-RH receptors is not fully understood and the inhibitory effects of Cetrorelix and bombesin antagonists on DU-145 tumour growth might be attributed at least in part to a downregulation of EHF receptors. Since Cetrorelix and bombesin antagonists inhibit growth of androgen-independent DU-145 prostate cancers, these compounds could be considered for the therapy of advanced prostate cancer in men, especially after relapse.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:European Journal of Cancer. - 33 : 7 (1997), p. 1141-1148. -
További szerzők:Pinski, Jacek Galvan, Georg Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Szepesházi Károly Cai, Ren-Zhi Groot, Kate Vadillo-Buenfil, Manuel Schally, Andrew Victor
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5.

001-es BibID:BIBFORM033650
Első szerző:Kahán Zsuzsa
Cím:Inhibition of growth of MDA-MB-468 estrogen-independent human breast carcinoma by bombesin/gastrin-releasing peptide antagonists RC-3095 and RC-3940-II / Zsuzsanna Kahán, Baodong Sun, Andrew V. Schally, José M. Arencibia, Ren-Zhi Cai, Kate Groot, Gábor Halmos
Dátum:2000
ISSN:0008-543X
Megjegyzések:BACKGROUND: The growth of breast carcinoma is promoted by autocrine growth factors such as the bombesin (BN)-like peptides and epidermal growth factor (EGF). The stimulatory action of BN-like peptides can be blocked by the use of BN/gastrin-releasing peptide (GRP) antagonists. METHODS: The authors investigated the effects of synthetic BN/GRP antagonists RC-3095 and RC-3940-II on tumor growth and the expression of mRNA for EGF receptors and three BN receptor subtypes in MDA-MB-468 human breast carcinoma. Athymic nude mice with xenografts of MDA-MB-468 human breast carcinoma were injected subcutaneously for 6 weeks with RC-3940-II at doses of 20 or 40 microg/day. In another study, the effects of RC-3940-II and RC-3095 were compared. RESULTS: RC-3940-II caused a significant and dose-dependent growth inhibition of MDA-MB-468 tumors in nude mice; therapy with either dose of RC-3940-II significantly (P<0.01) reduced the mean final tumor volume and weight compared with controls. RC-3940-II induced a persistent regression of > 50% of all tumors. One of 3 tumors treated with 20 microg of RC-3940-II and 3 of 5 tumors treated with 40 microg were found to have regressed completely by the end of the study. When RC-3940-II and RC-3095 were compared at the dose of 20 microg/day, both powerfully suppressed growth of MDA-MB-468 tumors, with RC-3940-II causing a complete regression of 2 tumors and RC-3095 a complete regression of 1 tumor. Receptor analyses of untreated MDA-MB-468 tumors revealed an overexpression of EGF receptors and two classes of binding sites for BN/GRP. mRNAs for receptors of GRP, neuromedin B, and BN receptor subtype-3 were detected by reverse transcriptase-polymerase chain reaction. CONCLUSIONS: A virtual arrest of growth or regression of MDA-MB-468 human breast carcinoma after therapy with RC-3940-II and RC-3095 indicates that these BN/GRP antagonists could provide a new treatment modality for breast tumors expressing BN and EGF receptors.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cancer. - 88 : 6 (2000), p. 1384-1392. -
További szerzők:Sun, Baodong Schally, Andrew Victor Arencibia, José M. Cai, Ren-Zhi Groot, Kate Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus)
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6.

001-es BibID:BIBFORM033583
035-os BibID:PMID:15655413 WOS:000227099800007
Első szerző:Kanashiro, Celia A.
Cím:Antagonists of bombesin/gastrin-releasing peptide decrease the expression of angiogenic and anti-apoptotic factors in human glioblastoma / Celia A. Kanashiro, Andrew V. Schally, R.-Z. Cai, Gabor Halmos
Dátum:2005
ISSN:0959-4973
Megjegyzések:We have investigated the antitumor effects and the mechanism of action of antagonists of bombesin/gastrin-releasing peptide (GRP), RC-3940-II and RC-3940-Et, on the growth of U-118MG human malignant glioma xenografted into nude mice. Tumors volume was measured weekly, and after 6 weeks of treatment with GRP antagonists the tumors were analyzed by Western blot assays for the expression of vascular endothelial growth factor (VEGF), protein kinase C (PKC)-alpha, the anti-apoptotic protein Bcl-2 and the pro-apoptotic protein Bax. A radioreceptor assay was used to characterize the receptors for bombesin/GRP. Specific high-affinity receptors for bombesin were found in U-118MG tumors, and their growth was reduced by 52.5% by RC-3940-II and 72.6% by RC-3940-Et (both p<0.01). The tumor doubling time was prolonged by 4.6 and 12 days after treatment with RC-3940-II and RC-3940-Et, respectively, compared to controls (p<0.05). Both antagonists caused a significant (p<0.05) decrease of about 28% in the levels of VEGF protein and a reduction of approximately 35% in the expression of PKCalpha. The relative ratio of Bcl-2:Bax was also diminished by around 70% by both analogs, indicating a net apoptotic gain and the efficacy of treatment. Our results suggest that bombesin/GRP antagonists, RC-3940-II and RC-3940-Et, could be of value for the treatment of human glioblastomas.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Anti-Cancer Drugs. - 16 : 2 (2005), p. 159-165. -
További szerzők:Schally, Andrew Victor Cai, Ren-Zhi Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus)
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7.

001-es BibID:BIBFORM033673
035-os BibID:PMID:9713279 WOS:000073781500024
Első szerző:Miyazaki, Masahiro
Cím:Inhibition of growth of MDA-MB-231 human breast cancer xenografts in nude mice by bombesin/gastrin-releasing peptide (GRP) antagonists RC-3940-II and RC-3095 / M. Miyazaki, N. Lamharzi, A. V. Schally, G. Halmos, K. Szepeshazi, K. Groot, R. Z. Cai
Dátum:1998
ISSN:0959-8049
Megjegyzések:Bombesin or gastrin-releasing peptide (GRP) may act as autocrine growth factors and play a role in the initiation and progression of breast cancer. We investigated the effect of bombesin/GRP antagonists RC-3095 and RC-3940-II on the growth of the MDA-MB-231 oestrogen-independent human breast cancer cell line xenografted into female nude mice. Bombesin/GRP antagonists, RC-3095 and RC-3940-II, were administered subcutaneously twice daily at a dose of 10 micrograms for 5 weeks. The growth of MDA-MB-231 tumours was inhibited during the treatment, as shown by a reduction in tumour volume. RC-3940-II and RC-3095 significantly decreased the final tumour volume by 72.4% and 57.7%, respectively, and greatly reduced tumour weights. RC-3940-II also significantly increased tumour doubling time and appeared to be more effective than RC-3095 in inhibiting the growth of MDA-MB-231 breast cancers. Serum gastrin and insulin-like growth factor-I (IGF-I) levels in animals treated with RC-3095 or RC-3940-II showed no significant changes as compared with controls. There was a significant decrease in the number of binding sites for epidermal growth factor (EGF), as well as bombesin, in tumour cells after chronic treatment with RC-3095 or RC-3940-II, which might be related to inhibition of tumour growth. Reverse transcription polymerase chain reaction, followed by Southern blot analysis, also showed a reduction in the expression of mRNA for EGF receptors in the group treated with RC-3940-II. Our findings suggest that bombesin/GRP antagonists such as RC-3095 or RC-3940-II could be considered for endocrine therapy for oestrogen-independent breast cancers, but further investigations are necessary.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:European Journal of Cancer. - 34 : 5 (1998), p. 710-717. -
További szerzők:Lamharzi, Najib Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Szepesházi Károly Groot, Kate Cai, Ren-Zhi
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8.

001-es BibID:BIBFORM033690
035-os BibID:WOS:A1997WD88500051
Első szerző:Nagy Attila
Cím:Design, synthesis, and in vitro evaluation of cytotoxic analogs of bombesin-like peptides containing doxorubicin or its intensely potent derivative, 2-pyrrolinodoxorubicin / Attila Nagy, Patricia Armatis, Ren-Zhi Cai, Karoly Szepeshazi, Gabor Halmos, Andrew V. Schally
Dátum:1997
ISSN:0027-8424
Megjegyzések:Five peptide fragments, based on the C-terminal sequence of bombesin (BN)-(6-14) or BN-(7-14), were selected as carriers for radicals doxorubicin (DOX) and 2-pyrrolino-DOX to create hybrid cytotoxic analogs. All these compounds had a reduced peptide bond (CH2-NH or CH2-N) between positions 13 (Phe or Leu) and 14 (Phe, Leu, or Tac) (Tac = thiazolidine-4-carboxylic acid). Three pseudononapeptide carriers contained N-terminal D-Phe or D-Tpi at position 6 (Tpi = 2,3,4,9-tetrahydro-1H-pyrido [3,4-b]indole-3-carboxylic acid). Two pseudooctapeptides had Gln(7) at the N terminus. The conjugation of N-(9-fluorenylmethoxycarbonyl)doxorubicin (N-Fmoc-DOX)-14-O-hemiglutarate to the peptide carriers at the N terminus resulted in cytotoxic hybrids of BN-like peptides containing DOX. These hybrids could then be converted to analogs with 2-pyrrolino-DOX by a reaction with 4-iodobutyraldehyde. The ability of the carriers and the conjugates to inhibit the binding of I-125-labeled [Tyr(4)]BN to receptors for BN/gastrin releasing peptide (GRP) on Swiss 3T3 cells was determined. Cytotoxic conjugates of pseudooctapeptide carrier analogs displayed the highest binding affinity (KD approximate to 1 nM). The cytotoxic BN analogs and their corresponding cytotoxic radicals exerted similar inhibitory effects on the in vitro growth of CFPAC-1 human pancreatic cancer, DMS-53 human lung cancer, PC-3 human prostate cancer, and MKN-45 human gastric cancer cell lines that have receptors for BN/GRP. In DMS-53 cells, the activity of 2-pyrrolino-DOX and its conjugates was approximate to 2500 times higher than that of DOX and its hybrids. These highly potent cytotoxic analogs of BN have been designed as targeted anti-tumor agents for the treatment of various cancers that possess receptors for BN/GRP.
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. - 94 : 2 (1997), p. 652-656. -
További szerzők:Armatis, Patricia Cai, Ren-Zhi Szepesházi Károly Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Schally, Andrew Victor
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9.

001-es BibID:BIBFORM033667
035-os BibID:WOS:000072115900079
Első szerző:Nagy Attila
Cím:Synthesis and biological evaluation of cytotoxic analogs of somatostatin containing doxorubicin or its intensely potent derivative, 2-pyrrolinodoxorubicin / Attila Nagy, Andrew V. Schally, Gábor Halmos, Patricia Armatis, Ren-Zhi Cai, Valér Csernus, Magdolna Kovács, Miklós Koppán, Károly Szepesházi, Zsuzsanna Kahán
Dátum:1998
ISSN:0027-8424
Megjegyzések:To create cytotoxic hybrid analogs of somatostatin (SST), octapeptides RC-160 (D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2) and RC-121 (D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NB2) were linked to doxorubicin (DOX) or its superactive derivative, 2-pyrrolino-DOX (AN-201). The conjugation was performed by coupling N-9-fluorenylmethoxycarbonyl (N-Fmoc)-DOX-14-O-hemiglutarate or 2-pyrrolino-DOX-14-O-hemiglutarate to the amino terminus of [Lys(Fmoc)(5)]RC-160 yielding AN-163 and AN-258, respectively, after deprotection. The respective cytotoxic conjugates of RC-121 (AN-162 and AN-238) were prepared similarly, In vitro tests on human cancer cell lines-MKN-45 gastric cancer, MDA-MB-231 breast cancer, PC-3 prostate cancer, and MIA PaCa-2 pancreatic cancer-demonstrated that the antiproliferative activity of the cytotoxic radicals in these conjugates,vas virtually retained. In H-345 human small cell lung carcinoma cell line, conjugates of RC-121 preserved the cytotoxic activity of their radicals, but the hybrids with RC-160 showed approximate to 10 times lower activity. The ability of the carriers and the hybrids to inhibit the binding of I-125-labeled RC-160 to receptors for SST on rat pituitary membrane preparation was also determined. The cytotoxic conjugates inhibited 50% of the specific binding of the radioligand in the nanomolar concentration range (IC50 < 80 nM). When SST-like activities of AN-238 and its carrier, RC-121, were compared in the rat pituitary superfusion system, both compounds were found to suppress a stimulated growth hormone release at nanomolar concentrations. Preliminary studies in animal models of breast and prostate cancers showed that AN-238 is less toxic than AN-201 and more potent in inhibiting tumor growth. These highly active cytotoxic analogs of SST have been designed as targeted antitumor agents for the treatment of various cancers expressing receptors for SST octapeptides.
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. - 95 : 4 (1998), p. 1794-1799. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Armatis, Patricia Cai, Ren-Zhi Csernus Valér J. Kovács Magdolna Koppán Miklós Szepesházi Károly Kahán Zsuzsa
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10.

001-es BibID:BIBFORM033886
035-os BibID:PMID:7947094
Első szerző:Pinski, Jacek
Cím:Effects of somatostatin analogue RC-160 and bombesin/gastrin-releasing peptide antagonists on the growth of human small-cell and non-small-cell lung carcinomas in nude mice / J. Pinski, A. V. Schally, G. Halmos, K. Szepeshazi, K. Groot, K. O'Byrne, R.-Z. Cai
Dátum:1994
ISSN:0007-0920
Megjegyzések:We investigated the effects of our synthetic bombesin/gastrin-releasing peptide (GRP) antagonists and somatostatin analogue RC-160 on the growth of human small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (non-SCLC) lines in nude mice. Athymic nude mice bearing xenografts of the SCLC NCl-H69 line or non-SCLC NCl-H157 line were treated for 5 and 4 weeks, respectively, with somatostatin analogue RC-160 or various bombesin/GRP antagonists. RC-160, administered s.c. peritumorally at a dose of 100 micrograms per animal per day, inhibited the growth of H69 SCLC xenografts as shown by more than 70% reduction in tumour volumes and weights, as compared with the control group. Bombesin/GRP antagonists, RC-3440, RC-3095 and RC-3950-II, given s.c. peritumorally at a dose of 20 micrograms per animal per day, also inhibited the growth of H69 SCLC tumours. RC-3950-II had the greatest inhibitory effect and decreased tumour volume and weights by more than 80%. The growth of H-157 non-SCLC xenografts was significantly reduced by treatment with RC-160, but not with bombesin/GRP antagonist RC-3095. In mice bearing either tumour model, administration of RC-160 significantly decreased serum growth hormone and gastrin levels. Specific high-affinity receptors for bombesin and somatostatin were found on membranes of SCLC H69 tumours, but not on non-SCLC H157 tumours. Receptor analyses demonstrated high-affinity binding sites for epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I) on the membranes of H69 and H157 tumours. EGF receptors were down-regulated on H69 tumours after treatment with RC-160 and bombesin/GRP antagonists. The concentration of binding sites for EGF and IGF-I on the H157 tumours was decreased after treatment with RC-160, but bombesin/GRP antagonist RC-3095 had no effect. These results demonstrate that bombesin/GRP antagonists inhibit the growth of H-69 SCLC, but not of H-157 non-SCLC xenografts in nude mice, whereas somatostatin analogue RC-160 is effective in both tumour models. This raises the possibility that these peptide analogues could be used selectively in the treatment of various subclasses of lung cancer.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:British Journal Of Cancer. - 70 : 5 (1994), p. 886-892. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Szepesházi Károly Groot, Kate O'Byrne, K. Cai, Ren-Zhi
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

001-es BibID:BIBFORM033897
035-os BibID:PMID:8313359 WOS:A1994MW68600033
Első szerző:Qin, Yunfeng
Cím:Inhibitory effect of bombesin receptor antagonist RC-3095 on the growth of human pancreatic cancer cells in vivo and in vitro / Yunfeng Qin, Tibor Ertl, Ren-Zhi Cai, Gabor Halmos, Andrew V. Schally
Dátum:1994
Megjegyzések:In this study, we investigated the effect of bombesin/GRP antagonist RC-3095 on the growth of CFPAC-1 human pancreatic cancer cells transplanted to nude mice or cultured in vitro. Nude mice bearing xenografts of the CFPAC-1 cell line received s.c. injections of RC-3095 (10 micrograms twice a day) or the vehicle (control) for 25 days. Chronic administration of RC-3095 inhibited the growth of CFPAC-1 tumors in nude mice as shown by a significant decrease in tumor volume throughout the period of treatment. Tumor volume doubling time was prolonged by RC-3095 treatment from 7.2 days to 10 days, and the tumor growth rate was decreased by 49%. In mice treated with RC-3095, the tumor growth delay time was 5.8 days. Treatment with RC-3095 decreased the final tumor weight by 37% and reduced DNA and protein contents in tumor tissues by 44 and 39.9%, respectively, compared to the controls. In cultures of the CFPAC-1 cell line, the addition of bombesin(1-14) (1 pM-0.1 microM) to the medium induced a dose-dependent increase in cell number. RC-3095 at 1 nM concentration effectively inhibited the bombesin-stimulated growth of CFPAC-1 cells in cultures. In the presence of 1 microM RC-3095 in the culture medium, the bombesin-induced growth of CFPAC-1 cells was totally suppressed. Bombesin was also shown to stimulate the DNA synthesis in CFPAC-1 cells in vitro as based on [3H]thymidine incorporation assay. When the cells were cultured in the presence of 1-100 nM bombesin, the uptake of [3H]thymidine by the cells was increased by 89-131%. RC-3095 inhibited both the basal and bombesin-stimulated DNA synthesis of CFPAC-1 cells. Addition of RC-3095 (10-100 nM) alone to the cultures caused a 39-40% decrease in the [3H]thymidine incorporation by the cells. Concomitant addition of RC-3095 (1 microM) and bombesin (1-100 nM) to the cultures induced a significant reduction in the uptake of [3H]thymidine by the cells compared to the values obtained with bombesin alone. Receptor binding assays showed the presence of two classes of specific binding sites for bombesin on CFPAC-1 cells, one with high affinity (Kd = 4.25 +/- 0.77 nM) and low capacity (Bmax = 0.268 +/- 0.052 pmol/10(6) cells) and the other with low affinity (Kd = 321.70 +/- 68.46 nM) and high capacity (Bmax = 3.991 +/- 0.374 pmol/10(6) cells).
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cancer research. - 54 : 4 (1994), p. 1035-1041. -
További szerzők:Ertl Tibor Cai, Ren-Zhi Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Schally, Andrew Victor
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM033893
035-os BibID:PMID:8045917
Első szerző:Qin, Yunfeng
Cím:Bombesin antagonists inhibit in vitro and in vivo growth of human gastric cancer and binding of bombesin to its receptors / Yunfeng Qin, Gabor Halmos, Ren-Zhi Cai, Balazs Szoke, Tibor Ertl, Andrew V. Schally
Dátum:1994
ISSN:0171-5216
Megjegyzések:We investigated the effect of bombesin/gastrin-releasing peptide (GRP) antagonist RC-3095 and other analogs on the growth of Hs746T human gastric cancer cells implanted in nude mice or cultured in vitro and on the binding of bombesin to its receptors. Nude mice bearing xenografts of the Hs746T cell line received s.c. injections of RC-3095 (10 micrograms twice daily) or the vehicle (control) for 21 days. Administration of antagonist RC-3095 inhibited the growth of Hs746T tumors. Treatment with RC-3095 produced a significant decrease in tumor volume, prolonged the tumor volume doubling time from 3.6 days to 5.1 days, and decreased the tumor growth rate by 76.9%. The tumor growth delay time in mice treated with RC-3095 was 2.8 days. Treatment with RC-3095 also decreased the final tumor weight by 88.3% and reduced DNA and protein contents in tumors by 91.5% and 89.5%, respectively, as compared to controls. The presence of specific receptors for bombesin/GRP was investigated on the crude membranes of implanted tumors of Hs746T cells. Saturation binding assays showed that the binding of [125I-Tyr4]bombesin to the membranes was saturable and reversible. Scatchard analysis indicated the presence of a single class of binding sites with a high affinity (Kd = 0.24 +/- 0.07 nM) and a low binding capacity (Bmax = 57.0 +/- 0.9 fmol/mg protein). In displacement studies, the binding of [125I-Tyr4]bombesin was inhibited in a dose-dependent manner by unlabelled bombesin(1-14), [Tyr4]-bombesin and GRP (14-27), but not by structurally unrelated peptides. Synthetic bombesin/GRP antagonists RC-3095, RC-3110, and RC-3950-II were all able to inhibit effectively the binding of [125I-Tyr4]bombesin to the membranes of Hs746T cells. RC-3950-II showed a higher binding affinity for bombesin receptors than RC-3095 or RC-3110. Addition of the non-hydrolyzable guanine-nucleotide analog GTP [S] to the binding buffer caused a significant reduction in the amount of [125I-Tyr4]bombesin bound to the cells, indicating that the bombesin receptor is coupled to a G-protein. In cell cultures, bombesin significantly stimulated the growth of Hs746T cells in vitro as shown by an increase in the uptake of [3H]thymidine. Bombesin antagonist RC-3095 could effectively inhibit the bombesin-stimulated growth of Hs746T cells in cultures. These observations suggest that bombesin/GRP may act as growth factors through specific receptors present on the membranes of Hs746T cells. Bombesin/GRP antagonists appear to nullify the effects of bombesin/GRP and may be useful for the treatment of gastric cancers.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Cancer Research And Clinical Oncology. - 120 : 9 (1994), p. 519-528. -
További szerzők:Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Cai, Ren-Zhi Szőke Balázs Ertl Tibor Schally, Andrew Victor
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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