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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
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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
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2.

001-es BibID:BIBFORM033598
035-os BibID:WOS:000185548300031
Első szerző:Bajo, Ana-Maria
Cím:Targeted doxorubicin-containing luteinizing hormone-releasing hormone analogue AN-152 inhibits the growth of doxorubicin-resistant MX-1 human breast cancers / Ana M. Bajo, Andrew V. Schally, Gabor Halmos, Attila Nagy
Dátum:2003
Megjegyzések:Purpose: The receptors for luteinizing hormone-releasing hormone receptor (LHRH-R) are found in >50% of human breast cancers. Doxorubicin (DOX) was linked to [D-Lys(6)]LHRH to form a cytotoxic conjugate, AN-152, which can be targeted to tumor cells expressing LHRH-R. We evaluated the effects of AN-152 on the estrogen-independent, DOX-resistant human mammary carcinoma line MX-1, xenografted into nude mice. Experimental Design: Nude mice bearing MX-1 tumors were administered five i.v. injections of AN-152 or DOX at doses equivalent to 3 mg/kg DOX. Tumor growth was followed, and changes in the expression of LHRH-R on tumors were evaluated by radioreceptor assays, reverse transcription-PCR, and Western blotting. The effects of AN-152 on the expression of human epidermal growth factor receptor (HER)-2 were investigated. Because LHRH-R are coupled to various G proteins, which are involved in mitogenic signaling, we determined the outcome of treatment with AN-152 on the levels of mRNA for different G proteins. Results: Treatment with AN-152 significantly (P < 0.05) decreased the final tumor volume to 978.56 +/- 176.85 mm(3), compared with the control tumors, which measured 2837.38 +/- 515.38 mm(3). Tumor doubling time was likewise significantly (P < 0.05) extended by AN-152 to 12.01 +/- 1.99 days from 6.45 +/- 0.36 days for the controls. Therapy with AN-152, but not with DOX, resulted in a significant decrease of LHRH-R levels on MX-1 tumors. The expression of mRNAs for HER-2, HER-3, Galpha(i2), and Galpha(11) and the levels of HER-2 and HER-3 proteins were also significantly reduced by AN-152. Conclusions: Cytotoxic LHRH analogue AN-152 could be considered for targeted chemotherapy of DOX-resistant breast cancers expressing LHRH-R.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Clinical Cancer Research. - 9 : 10 (2003), p. 3742-3748. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Nagy Attila
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3.

001-es BibID:BIBFORM033618
035-os BibID:WOS:000089931600051 PMID:11051271
Első szerző:Chatzistamou, Ioulia
Cím:Effective treatment of metastatic MDA-MB-435 human estrogen-independent breast carcinomas with a targeted cytotoxic analogue of luteinizing hormone-releasing hormone AN-207 / Ioulia Chatzistamou, Andrew V. Schally, Attila Nagy, Patricia Armatis, Karoly Szepeshazi, Gabor Halmos
Dátum:2000
Megjegyzések:A highly potent derivative of doxorubicin, 2-pyrrolinod-oxorubicin (AN-201), was linked to [D-Lys(6)]luteinizing hormone-releasing hormone (LH-RH) to form a cytotoxic analogue, AN-207, that can be targeted to LH-RT-I receptors, The effects of AN-207 were investigated in MDA-MB-435 human estrogen-independent breast carcinomas, which express LB-RH receptors, In experiment I, nude mice bearing orthotopically implanted tumors received a single i.v. injection of AN-207, AN-201, or the carrier at 250 nmol/kg, Five weeks after administration of AN-207, tumor volume was significantly decreased by 66% (P < 0.001) and tumor burden by 71% (P < 0.05) as compared with controls, but no significant effects occurred in other groups. Six of eight (75%) control animals and 37.5% of mice treated with AN-201 developed metastases in the lymph nodes, whereas no lymphatic spread was found in any of the mice that received injections of AN-207, The antitumor effect of AN-207 could be partially blocked by pretreatment of the tumor-bearing mice with high doses of agonist [D-Trp(6)]LH-RH,which suggests that AN-207 acts on LH-RH receptors on tumors. The mortality due to toxicity was 25% in the group receiving AN-201 and 12.5% in the AN-207-treated group. Radioligand binding assays revealed the presence of high-affinity binding sites for LH-RH on tumor membranes, and mRNA for LH-RH receptors was demonstrated by reverse transcription-PCR, In experiment 2, two i.v. injections of AN-207 or AN-201 at 150 nmol/kg were given on days 0 and 28 to mice bearing orthotopic xenografts of MDA-MB-435, The outcome of the treatment was similar to that observed in experiment 1, but without any toxicity-related deaths, Tumor growth inhibition and prevention of metastatic disease suggest that cytotoxic LH-RH analogue AN-207 could be considered for the treatment of human estrogen-independent breast cancers expressing receptors for LH-RH.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Clinical Cancer Research. - 6 : 10 (2000), p. 4158-4165. -
További szerzők:Schally, Andrew Victor Nagy Attila Armatis, Patricia Szepesházi Károly Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus)
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4.

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)
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5.

001-es BibID:BIBFORM033581
035-os BibID:WOS:000227770000039 PMID:15788692
Első szerző:Engel, Jörg B.
Cím:Effective inhibition of experimental human ovarian cancers with a targeted cytotoxic bombesin analogue AN-215 / Jörg B. Engel, Gunhild Keller, Andrew V. Schally, Gabor Halmos, Brian Hammann, Attila Nagy
Dátum:2005
ISSN:1078-0432
Megjegyzések:Purpose: To determine whether the cytotoxic analogue of bombesin/gastrin-releasing peptide (GRP) AN-215 can inhibit the in vivo growth of four human ovarian cancer cell lines. AN-215 consists of 2-pyrrolinodoxorubicin (AN-201), a superactive derivative of doxorubicin linked to a bombesin antagonist carrier des-D-Tpi-RC-3095. This conjugate binds strongly to receptors for bombesin/GRP and can be targeted to tumors that express these receptors. Bombesin/GRP receptors are found in 77% of human ovarian cancer specimens. Experimental Design: Nude mice bearing xenografts of ES-2, SKOV-3, OV-1063, and UCI-107 human ovarian carcinomas were treated with AN-215. The antitumor effects and the toxicity were determined. The expression of bombesin receptor subtypes was measured by reverse-transcriptase PCR analysis, and the presence of bombesin/GRP receptors was determined by radioligand binding assays. Results: AN-215 significantly (P < 0.05) inhibited growth of ES-2, OV-1063, and UCI-107 tumors, prevented the metastatic spread of ES-2 cancers, and prolonged the survival of nude mice bearing i.p. ES-2 xenografts. Cytotoxic radical AN-201, the unconjugated mixture of bombesin antagonist RC-3095 and AN-201 or RC-3095 alone had no significant effects. Blockade of bombesin/GPP receptors abolished the effect of AN-215. The expression of bombesin/GRP receptors was not changed after repeated treatment with AN-215. Conclusions: Our findings indicate that targeted chemotherapy with cytotoxic bombesin/GRP analogue AN-215 can inhibit ovarian tumors, which express bombesin/GRP receptors. AN-215 might provide a new treatment modality for women with advanced ovarian carcinoma.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Clinical Cancer Research. - 11 : 6 (2005), p. 2408-2415. -
További szerzők:Keller, Gunhild Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Hammann, Brian Nagy Attila
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6.

001-es BibID:BIBFORM033570
035-os BibID:PMID:16051478 WOS:000231891900035
Első szerző:Engel, Jörg B.
Cím:Experimental therapy of human endometrial cancers with a targeted cytotoxic bombesin analog AN-215 : low induction of multidrug resistance proteins / Jörg B. Engel, Andrew V. Schally, Gabor Halmos, Benjamin Baker, Attila Nagy, Gunhild Keller
Dátum:2005
ISSN:0959-8049
Megjegyzések:In this study we have investigated the efficacy and toxicity of targeted cytotoxic bombesin (BN) analog AN-215 and its effects on the expression of three multidrug resistance proteins in experimental human endometrial cancers. Nude mice bearing HEC-1A, RL-95-2 and AN3CA tumours were treated with AN-215 and its cytotoxic radical (AN-201). The BN receptor expression in tumours was followed by RT-PCR analysis and radioligand binding assays. Expression of drug resistance proteins MDR-1, MRP-1 and BCRP were measured by realtime PCR. AN-215 significantly (P<0.05) inhibited the growth of HEC-1A, RL-95-2 and AN3CA tumours while AN-201 was ineffective. The expression of BN receptors was demonstrated in all three tumour models. AN-215 caused a lower induction of MDR-1 in HEC-1A and RL-95-2 cancers than AN-201. MRP-1 and BCRP were not induced by AN-215 or AN-201. Thus, targeted chemotherapy with AN-215 powerfully inhibits the growth of human BN receptor-positive endometrial cancers.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:European Journal Of Cancer. - 41 : 12 (2005), p. 1824-1830. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Baker, Benjamin Nagy Attila Keller, Gunhild
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7.

001-es BibID:BIBFORM033564
035-os BibID:WOS:000231743700023 PMID:16047355
Első szerző:Engel, Jörg B.
Cím:Targeted therapy with a cytotoxic somatostatin analog, AN-238, inhibits growth of human experimental endometrial carcinomas expressing multidrug resistance protein MDR-1 / Jorg B. Engel, Andrew V. Schally, Gabor Halmos, Ben Baker, Attila Nagy, Gunhild Keller
Dátum:2005
ISSN:0008-543X
Megjegyzések:BACKGROUND. Chemoresistance mediated by membrane transporters such as multidrug resistance (MDR-1) glycoprotein remains a challenge in the chemotherapy treatment of advanced or recurrent endometrial carcinoma. Targeted chemotherapy might overcome this resistance. The cytotoxic somatostatin (SST) analog, AN-238, consists of a superactive derivative of doxorubicin (DOX), 2-pyrrolino-DOX (AN-201), linked to the SST analog carrier, RC-121. This conjugate binds strongly to SST receptor subtypes (sst) 2a (sst2(a)) and 5 (sst(5)) and can be targeted to tumors that express these receptors. METHODS. The presence of sst2(a) and sst, was determined in 3 human endometrial carcinoma cell lines (HEC-1A, RL-95-2, and AN3CA). Nude mice bearing xenografts of these cancers were treated with AN-238 and its radical, AN-201. The antitumor effects and toxicity were compared. The authors studied the effects of AN-238 and AN-201 on the expression levels of MDR-1, multidrug resistance related protein (MRP-1), and breast carcinoma resistance protein (BCRP) by real-time polymerase chain reaction. RESULTS. The authors demonstrated the presence of mRNA and receptor protein for sst2(a) and sst, on HEC-1A, RL-95-2, and AN3CA tumors. AN-238 significantly (P < 0.05) inhibited the growth of these tumors, whereas AN-201 had no effect. Blockade of SST receptors nullified the effects of AN-238. In all 3 endometrial carcinoma lines, AN-238 caused a weaker induction of MDR-1 than AN-201. No major induction of MRP-1 and BCRP occurred after treatment with AN-238 or AN-201. CONCLUSIONS. Targeted chemotherapy with the cytotoxic SST analog, AN-238, inhibited powerfully the growth of endometrial carcinoma, which express SST receptors, regardless of their expression level of MDR-1.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cancer. - 104 : 6 (2005), p. 1312-1321. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Baker, Benjamin Nagy Attila Keller, Gunhild
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8.

001-es BibID:BIBFORM033554
035-os BibID:WOS:000234215800022 PMID:16322338
Első szerző:Engel, Jörg B.
Cím:Targeted cytotoxic bombesin analog AN-215 effectively inhibits experimental human breast cancers with a low induction of multi-drug resistance proteins / Jörg B. Engel, Andrew V. Schally, Gabor Halmos, Benjamin Baker, Attila Nagy, Gunhild Keller
Dátum:2005
ISSN:1351-0088
Megjegyzések:The cytotoxic analog of bombesin (BN)/gastrin releasing peptide (GRP) AN-215 consisting of 2-pyrrolinodoxorubicin (AN-201), a superactive derivative of doxorubicin linked to a bombesin analog carrier, displays a high affinity to BN/GRP receptors and can be targeted to tumors that express these receptors. We evaluated the antitumor effect and the toxicity of AN-215 in 5 human breast cancer cell lines xenografted into nude mice. In addition, we measured the mRNA expression of multi drug resistance protein 1 (MDR-1), multi drug resistance related protein 1 (MRP-1) and breast cancer resistance protein (BCRP) by real-time PCR analysis after treatment with AN-215. All five cell lines expressed BN/GRP receptors, and AN-215 significantly (P<0.05) inhibited tumor growth in all models, while its cytotoxic radical AN-201 had no significant effect in four models. In MX-1 tumors, AN-201 had a significantly weaker antitumor effect than AN-215. The effect of AN-215 was nullified by a blockade of BN/GRP receptors with a bombesin antagonist. Low or no induction of MDR-1, MRP-1 and BCRP occurred after treatment with AN-215. In conclusion, targeted chemotherapy with the cytotoxic BN/GRP analog AN-215 strongly inhibits breast cancers that express BN/GRP receptors and might provide a new treatment modality for mammary carcinoma.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Endocrine-Related Cancer. - 12 : 4 (2005), p. 999-1009. -
További szerzők:Schally, Andrew Victor Halmos Gábor (1962-) (gyógyszerész, receptorfarmakológus, experimentális onkológus) Baker, Benjamin Nagy Attila Keller, Gunhild
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9.

001-es BibID:BIBFORM033894
035-os BibID:PMID:7923093 WOS:A1994PK64700016
Első szerző:Halmos Gábor (gyógyszerész, receptorfarmakológus, experimentális onkológus)
Cím:Characterization of bombesin/gastrin-releasing peptide receptors in membranes of MKN45 human gastric cancer / Gabor Halmos, Jacek Pinski, Balazs Szoke, Andrew V. Schally
Dátum:1994
ISSN:0304-3835
Megjegyzések:Binding of the radiolabeled bombesin analog [125I-Tyr4]bombesin to crude cell membranes of MKN45 human gastric cancer grown in nude mice was investigated in vitro. Scatchard analyses of multipoint binding data, performed by complete displacement method demonstrated the presence of two classes of [Tyr4]bombesin binding sites. The high-affinity binding sites had a mean dissociation constant (Kd1) of 2.75 nM with a mean maximal binding capacity (Bmax1) of 492 fmol/mg membrane protein, while the low-affinity binding sites showed a mean dissociation constant (Kd2) of 0.41 microM with a mean maximal binding capacity (Bmax2) of 41.4 pmol/mg membrane protein. Binding of [125(1)-Tyr4]bombesin was specific, reversible and linearly related to the protein concentration of tumor membrane. In displacement studies, the binding of radiolabeled [Tyr4]bombesin was inhibited in a dose-dependent manner by gastrin releasing peptide (GRP)(14-27) and two synthetic antagonists of bombesin/GRP, RC-3095 and RC-3950-II. Both antagonists exhibited high affinity in nearly the same concentration range as GRP(14-27). The presence of receptors for bombesin/GRP on human gastric cancer membranes suggests that bombesin-like peptides may play a role in growth of gastric cancer.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cancer Letters. - 85 : 1 (1994), p. 111-118. -
További szerzők:Pinski, Jacek Szőke Balázs Schally, Andrew Victor
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10.

001-es BibID:BIBFORM033846
035-os BibID:PMID:7812958 WOS:A1995QB80800014
Első szerző:Halmos Gábor (gyógyszerész, receptorfarmakológus, experimentális onkológus)
Cím:Characterization of bombesin/gastrin-releasing peptide receptors in human breast cancer and their relationship to steroid receptor expression / Gabor Halmos, James L. Wittliff, Andrew V. Schally
Dátum:1995
Megjegyzések:Bombesin (BN) and its mammalian counterpart, gastrin-releasing peptide (GRP), are hormonally active peptides which appear to function as autocrine or paracrine growth factors in a variety of cells. As part of a long-term investigation of the relationship of peptide and steroid hormone receptors to breast cancer progression and treatment, we examined the binding of [125I-Tyr4]BN to membranes isolated from 100 human breast carcinomas. Thirty-three of these tumors expressed BN/GRP receptor levels of > 10 fmol/mg membrane protein. Two classes of [Tyr4]BN-binding sites were detected using Scatchard analyses of radioligand association data from hormone displacement curves. The high-affinity binding sites exhibited a mean dissociation constant (Kd1) of 2.1 nM and a mean specific binding capacity (Bmax1) of 237 fmol/mg membrane protein. The low affinity binding sites had a mean dissociation constant (Kd2) of 0.3 microM and a mean binding capacity (Bmax2) of 5.9 pmol/mg membrane protein. BN/GRP receptor expression in a breast carcinoma was unrelated to patient age. When the levels of BN/GRP receptors were compared to the content of the sex steroid receptors, a highly significant positive correlation (P < 0.005) was observed between the binding capacities of high-affinity [Tyr4]BN-binding sites and estrogen receptor levels and between the concentrations of low affinity [Tyr4]BN-binding sites and progestin receptor levels (P < 0.05). This represents the first report of these labile, regulatory proteins in biopsies of human breast carcinomas. Expression of specific receptor proteins for BN/GRP, potent mitogens, in a large number of human breast cancers suggests that they may be involved in tumor cell progression. The approach based on determination of BN/GRP receptors might be useful to guide a hormonal therapy with BN/GRP antagonists in some women with breast cancer.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cancer Research. - 55 : 2 (1995), p. 280-287. -
További szerzők:Wittliff, James L. Schally, Andrew Victor
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11.

001-es BibID:BIBFORM033665
035-os BibID:PMID:10355741 WOS:000080006900002
Első szerző:Halmos Gábor (gyógyszerész, receptorfarmakológus, experimentális onkológus)
Cím:Cytotoxic analogs of luteinizing hormone-releasing hormone bind with high affinity to human breast cancers / Gabor Halmos, Attila Nagy, Najib Lamharzi, Andrew V. Schally
Dátum:1999
ISSN:0304-3835
Megjegyzések:Recently, we developed two new cytotoxic analogs of luteinizing hormone-releasing hormone (LH-RH), AN-152 in which doxorubicin (DOX) is linked to [D-Lys6]LH-RH, and AN-207 which consists of 2-pyrrolino-DOX coupled to [D-Lys6]LH-RH. In this study, we examined binding of AN-152 and AN-207 to membranes of human breast cancer specimens and MCF-7 and MDA-MB-231 human breast cancer lines. Both cytotoxic analogs displayed IC50 values in the nanomolar concentration range (IC50 = 2-13 nM). Using radioligand binding studies, we characterized the receptors for LH-RH on membranes of breast cancers. In addition, the expression of mRNA for LH-RH receptors in MCF-7 and MDA-MB-231 cell lines was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR). These highly active cytotoxic analogs of LH-RH have been designed as targeted chemotherapeutic agents for the treatment of various cancers expressing receptors for LH-RH.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cancer Letters. - 136 : 2 (1999), p. 129-136. -
További szerzők:Nagy Attila Lamharzi, Najib Schally, Andrew Victor
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12.

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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