CCL

Összesen 7 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM033615
035-os BibID:PMID:11272290 WOS:000166756100010
Első szerző:Arencibia, José M.
Cím:In vitro targeting of a cytotoxic analog of luteinizing hormone-releasing hormone AN-207 to ES-2 human ovarian cancer cells as demonstrated by microsatellite analyses / Jose M. Arencibia, Andrew V. Schally, Gabor Halmos, Attila Nagy, Hippokratis Kiaris
Dátum:2001
ISSN:0959-4973
Megjegyzések:Targeting of cytotoxic agents represents a modern approach to the treatment of various cancers, that improves the efficacy and reduces peripheral toxicity. Recently we developed a powerful cytotoxic analog of luteinizing hormone-releasing hormone (LHRH), AN-207, designed to be targeted to tumors that express LHRH receptors. This analog consists of the superactive derivative of doxorubicin (DOX), 2-pyrrolino-DOX (AN-201), linked to [D-Lys6]LHRH carrier. In the present study we investigated the cytocidal effects of AN-207 and AN-201 on the LHRH receptor-positive ES-2 ovarian cancer cells. The targeting of AN-207 to ES-2 cells in the presence of LHRH receptor-negative UCI-107 ovarian cancer cells was also evaluated by semi-quantitative polymerase chain reaction (PCR) amplification of microsatellite markers. Ligand competition assays showed a single class of high-affinity and low-capacity binding sites in ES-2 cells with a mean dissociation constant (KD) of 3.93 +/- 0.1 nM and a mean maximal binding capacity (Bmax) of 271 +/- 26.1 fmol/mg membrane protein. Kinetic assays indicated that AN-207 caused cell death in a concentration- and time-dependent manner in ES-2 cells, but not in UCI-107 cells, while the kinetics of cytotoxic effects of AN-201 were similar in both cell lines. To investigate targeting, ES-2 cells were co-cultured with UCI-107 cells, treated with 10 nM AN-207 or AN-201 for different times and then cultured for 48 h in the absence of cytotoxic agents. Genomic DNA was extracted for microsatellite analyses using different markers. Semi-quantitative analyses of the intensity of the alleles that correspond to each cell line indicated that AN-207 was selectively targeted to ES-2 cells, while AN-201 showed no selectivity for either cell line. These results extend our previous findings that AN-207 can be targeted to ovarian cancers and other tumors that express receptors for LHRH. Cytotoxic analogs of LHRH, such as AN-207, should be considered for treatment of LHRH receptor-positive tumors.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Anti-Cancer Drugs. - 12 : 1 (2001), p. 71-78. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Nagy Attila Kiaris, Hippokratis
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

2.

001-es BibID:BIBFORM033608
035-os BibID:PMID:11593058 WOS:000171913800008
Első szerző:Chatzistamou, Ioulia
Cím:Inhibition of growth and metastases of MDA-MB-435 human estrogen-independent breast cancers by an antagonist of growth hormone-releasing hormone / Ioulia Chatzistamou, Andrew V. Schally, Jozsef L. Varga, Kate Groot, Rebeca Busto, Patricia Armatis, Gabor Halmos
Dátum:2001
ISSN:0959-4973
Megjegyzések:Antagonists of growth hormone-releasing hormone (GH-RH) inhibit the growth of various cancers by mechanism(s) that include the suppression of the insulin-like growth factors (IGF)-I and/or -II. In this study, nude mice bearing orthotopic implants of MDA-MB-435 human estrogen-independent breast carcinoma received 39 days of therapy with GH-RH antagonist JV-1-36 (20 microg/day). The treatment significantly inhibited tumor growth by 71.1% (p<0.01) and nullified the metastatic potential of MDA-MB-435 cells. Four of eight control mice (50%) developed metastases in the lymph nodes and one (12.5%) in the lung, but none of the animals receiving JV-1-36 showed metastatic spread. GH-RH antagonist JV-1-36 inhibited the growth of MDA-MB-435 cells in vitro, while IGF-I stimulated it. However, mRNA for IGF-I or -II was not detected in MDA-MB-435 cells, indicating that the suppression of autocrine IGFs may not be involved in the antiproliferative mechanism. Using ligand competition assays with (125)I-labeled GH-RH antagonist JV-1-42, specific high-affinity binding sites for GH-RH were found on tumor membranes. Reverse transcription-polymerase chain reaction revealed the expression of mRNA for GH-RH receptor splice variant-1 in MDA-MB-435 tumors. Our results suggest that the antitumorigenic action of GH-RH antagonists on MDA-MB-435 breast cancer could be direct and mediated by tumoral GH-RH receptors.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Anti-Cancer Drugs. - 12 : 9 (2001), p. 761-768. -
További szerzők:Schally, Andrew Victor Varga József L. Groot, Kate Busto, Rebeca Armatis, Patricia Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

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)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

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
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

5.

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
Borító:

6.

001-es BibID:BIBFORM033757
035-os BibID:PMID:9436641 WOS:A1997YK13000009
Első szerző:Szepesházi Károly
Cím:Targeted cytotoxic luteinizing hormone releasing hormone (LH-RH) analogs inhibit growth of estrogen independent MXT mouse mammary cancers in vivo by decreasing cell proliferation and inducing apoptosis / Károly Szepeshazi, Andrew V. Schally, Attila Nagy, Gábor Halmos, Kate Groot
Dátum:1997
Megjegyzések:Tumor inhibitory action and the optimal dosage regimens of highly potent targeted cytotoxic luteinizing hormone releasing hormone (LH-RH) analogs containing doxorubicin (DOX) or 2-pyrrolino-DOX (AN-201) were tested in female BDF mice bearing estrogen independent MXT mouse mammary cancers. The effects were compared to those obtained with the cytotoxic radicals DOX or AN-201 alone. Analog AN-207, formed by linking 2-pyrrolino-DOX to [D-Lys6]LH-RH, and analog AN-152, produced by conjugation of DOX to the same carrier, given i.p. as a single injection or repeatedly 2 days apart at their maximum tolerated doses (MTDs) resulted in a 89-93% inhibition of tumor growth. Equimolar amounts of the cytotoxic radicals were toxic. AN-207 and AN-152 likewise had stronger tumor inhibitory effects than their respective cytotoxic radicals AN-201 or DOX alone, when compared at the lower doses corresponding to MTDs of the radicals. Histological evaluation indicated that decreased cell proliferation (shown by mitotic index and AgNOR counts) as well as increased apoptosis (demonstrated by histological and biochemical methods) both contributed to tumor suppression caused by the cytotoxic hormone analogs. Specific, high-affinity LH-RH receptors were present on MXT tumor samples of control untreated mice, but no binding sites for LH-RH could be found on tumor membranes after treatment with the cytotoxic LH-RH analogs. The results suggest that these powerful targeted cytotoxic LH-RH analogs could be considered for treatment of human mammary cancers having receptors for LH-RH.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Anti-Cancer Drugs. - 8 : 10 (1997), p. 974-987. -
További szerzők:Schally, Andrew Victor Nagy Attila Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Groot, Kate
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM005445
Első szerző:Szepesházi Károly
Cím:Therapy of experimental hepatic cancers with cytotoxic peptide analogs targeted to receptors for luteinizing hormone-releasing hormone, somatostatin or bombesin / Károly Szepesházi, Andrew V. Schally, Andrea Treszl, Stephan Seitz, Gábor Halmos
Dátum:2008
Megjegyzések:As there is no effective systemic therapy for advanced hepatocellular carcinoma (HCC), we investigated the presence of receptors for somatostatin, bombesin and luteinizing hormone-releasing hormone (LHRH) in SK-Hep-1 human hepatic carcinoma and the effects of cytotoxic analogs of somatostatin (AN-238), bombesin (AN-215) and LHRH (AN-207) on the growth of this tumor. Nude mice bearing SK-Hep-1 HCCs were treated with AN-238, AN-215, AN-207 and their combination, or cytotoxic radical 2-pyrrolinodoxorubicin (AN-201). Tumor growth reduction was determined and cell proliferation characteristics and apoptosis were studied by histologic analysis. The expression of receptors for somatostatin, bombesin and LHRH was investigated by radioreceptor assays and immunohistochemistry. High-affinity binding sites for somatostatin, bombesin and LHRH were detected in SK-Hep-1 cancers. All three cytotoxic peptide analogs inhibited growth of SK-Hep-1 tumors and decreased the cell proliferation rate. Combination therapy with two or three cytotoxic analogs resulted in the strongest tumor inhibition. Receptors for somatostatin, bombesin and LHRH are expressed in SK-Hep-1 human HCC. Cytotoxic peptide analogs targeted to these receptors inhibit growth of this tumor. Targeting to multiple receptors enhances the efficacy of therapy. The results of our study encourage additional experimental investigations to permit the introduction of these cytotoxic analogs into clinical trials.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Anti-Cancer Drugs. - 19 : 4 (2008), p. 349-358. -
További szerzők:Schally, Andrew Victor Treszl Andrea (1974-) (molekuláris biológus) Seitz, Stephan Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus)
Internet cím:DOI
elektronikus változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.