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  • 1
    Electronic Resource
    Electronic Resource
    Antagonists of growth hormone-releasing hormone arrest the growth of MDA-MB-468 estrogen-independent human breast cancers in nude mice (2000)
    Springer
    Breast cancer research and treatment 60 (2000), S. 71-79 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; growth hormone-releasing hormone (GH-RH) antagonists ; IGF-I ; IGF-I receptor ; GH-RH
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Since antagonists of growth hormone-releasing hormone (GH-RH) inhibit proliferation of various tumors, in this study we investigated the effects of GH-RH antagonists MZ-5-156 or JV-1-36 on growth of estrogen-independent MDA-MB-468 human breast cancers xenografted into nude mice. Both GH-RH antagonists administered at a dose of 20 μg/day induced regression of some and growth-arrest of other tumors, while control tumors continued to grow. After 5 weeks of therapy with MZ-5-156 or JV-1-36, final volume and weight of MDA-MB-468 tumors were significantly decreased (all p values 〈0.001) and serum IGF-I levels as well as tumor IGF-I mRNA expression were reduced as compared with controls. High affinity binding sites for IGF-I were detected by the ligand binding method. Gene expression of human IGF-I receptors, as measured by the RT-PCR, was not significantly different in control and treated MDA-MB-468 tumors. In cell culture, IGF-I did not stimulate, GH-RH slightly stimulated, while MZ-5-156 and JV-1-36 inhibited proliferation of MDA-MB-468 cells known to possess defective insulin and IGF-I receptor signaling. The expression of mRNA for human GH-RH was found in five of 8 tumors treated with GH-RH antagonists, and in one of the five control tumors. These results suggest that GH-RH antagonists inhibit MDA-MB-468 breast cancers possibly through mechanisms involving interference with locally produced GH-RH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006363230990
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Epidermal growth factor-like activity and epidermal growth factor-receptors in human primary breast cancer (1993)
    Springer
    Breast cancer research and treatment 26 (1993), S. 41-47 
    Details
    ISSN: 1573-7217
    Keywords: EGF-like activity ; EGF-receptor ; prognostic factors in breast cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ligands binding to epidermal growth factor-receptors (EGF-Rs) as epidermal growth factor-like activity (EGF-like activity), along with EGF-R levels, were determined from human primary breast cancer samples. Receptor analysis revealed a single class of high affinity binding sites. Ng/mg protein EGF-like activity quantities were measured in cytosols, and were inversely correlated with EGF-R contents (p 〈 0.01), estimated by two-point assays.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00682698
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Administration of a targeted cytotoxic analog of luteinizing hormone-releasing hormone inhibits growth of estrogen-independent MDA-MB-231 human breast cancers in nude mice (2000)
    Springer
    Breast cancer research and treatment 59 (2000), S. 255-262 
    Details
    ISSN: 1573-7217
    Keywords: cytotoxic LH-RH analog ; estrogen-independent breast cancer ; LH-RH receptors ; MDA-MB-231 xenografts ; receptor targeted chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Receptor targeted chemotherapy is less toxic and more effective than conventional chemotherapy. Receptors for luteinizing hormone-releasing hormone (LH-RH) are found in about 50% of human breast cancers. Highly potent cytotoxic radical 2-pyrrolinodoxorubicin (AN-201) was linked to the agonistic analog [D-Lys6]LH-RH to form cytotoxic LH-RH analog AN-207. We evaluated whether AN-207 could be targeted to the hormone-independent MDA-MB-231 human breast cancers. Nude mice bearing MDA-MB-231 tumors were injected i.v. with 250 nmol/kg doses of cytotoxic radical AN-201, cytotoxic LH-RH analog AN-207, the unconjugated mixture of AN-201 and carrier [D-Lys6]LH-RH, [D-Lys6]LH-RH alone and vehicle (control). The growth of MDA-MB-231 tumors in animals given a single dose of AN-207 was inhibited significantly (p=0.01) for 3 weeks after injection, whereas tumors in all the other groups grew steadily. All cytotoxic compounds produced leukopenia, but the strongest lymphocyte suppression was caused by cytotoxic radical AN-201. Three weeks after treatment, the presence of mRNA for LH-RH receptors was demonstrated by RT-PCR in all the groups and radioreceptor assays demonstrated high-affinity binding sites for LH-RH on tumor cell membranes of control animals and those treated with AN-201, the carrier peptide alone or in combination with AN-201. At this time point binding assays did not reveal the expression of membrane proteins in tumors treated with AN-207, but 60 days after administration of AN-207, high affinity LH-RH binding sites were found again in MDA-MB-231 tumors. These results indicate that cytotoxic LH-RH analog AN-207 could be utilized for receptor targeted chemotherapy of breast cancers expressing receptors for LH-RH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006352401912
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    Paper (German National Licenses)
    Fulltext
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