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  • 1
    Electronic Resource
    Electronic Resource
    Growth inhibition of experimental pancreatic cancers and sustained reduction in epidermal growth factor receptors during therapy with hormonal peptide analogs (1999)
    Springer
    Journal of cancer research and clinical oncology 125 (1999), S. 444-452 
    Details
    ISSN: 1432-1335
    Keywords: Key words Experimental pancreatic cancer ; Hormonal therapy ; Bombesin antagonist ; Somatostatin analog ; LH-RH antagonist ; EGF receptor ; Apoptosis ; AgNOR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Reduction in receptors for epidermal growth factor (EGF) in cancers appears to be one of the principal mechanisms through which peptide hormone analogs can inhibit tumor growth. In this study, hamsters with nitrosamine-induced pancreatic cancers were treated for 8 weeks with bombesin/gastrin-releasing peptide (GRP) antagonist RC-3095, somatostatin analog RC-160 or the luteinizing hormone-releasing hormone antagonist Cetrorelix, using sustained delivery systems releasing 20, 35 and 20 μg analog/ day respectively. To establish the pattern of changes in the number and affinity of EGF receptors on tumors, groups of animals were sacrificed at regular intervals during therapy. Chronic treatment with RC-3095 or Cetrorelix resulted in an early (day 10) and sustained reduction (71% or 69% respectively) in EGF receptors on pancreatic tumors. In contrast, RC-160 decreased receptor concentration by 60% only after 20 days. Among the histological characteristics of proliferation, the decrease in argyrophilic nucleolar organizer regions, but not apoptotic and mitotic indices, showed a correlation with the fall in EGF receptors. The concentration of the receptors returned to the control level 4 days after cessation of chronic treatment with RC-3095. The effect of single injections of RC-3095, RC-160 and Cetrorelix on EGF receptors was also investigated. RC-160 decreased the number of EGF receptors on pancreatic cancers by 31% 3 h after administration, but the receptors had returned to normal level at 6 h. RC-3095 and Cetrorelix caused a 67% and 59% decline, respectively, in EGF receptors only 6 h after injection and the concentration of receptors remained low for 24 h. Thus, the pattern of down-regulation of EGF receptors in pancreatic cancers appears to depend on the peptide used for therapy. Since the antitumor effect may be the result of the fall in EGF receptors in cancers, information on the time course of changes in these receptors during treatment with these analogs may lead to an improvement in therapeutic regimens.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004320050301
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  • 2
    Electronic Resource
    Electronic Resource
    Luminal gastric somatostatin-like immunoreactivity in response to various stimuli in man (1986)
    Springer
    Digestive diseases and sciences 31 (1986), S. 833-839 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study investigates release of somatostatin-like immunoreactivity (SLI) into the gastric lumen of five healthy human subjects in response to pharmacological stimuli (pentagastrin and secretin) and physiological stimuli (sham feeding and intrajejunal perfusion of elemental diet). Basal and poststimulation gastric juice aspirates were collected at 15-min intervals, extracted with acetone, and SLI determined by radioimmunoassay, with these results: (1) A considerable amount of SLI was secreted during the basal period. (2) Pentagastrin stimulated SLI release quickly and was associated with increased acid secretion. (3) Both secretin and sham feeding increased SLI only slightly. (4) During intrajejunal perfusion of the elemental diet, SLI increased significantly, was associated with decreased acid secretion, and rapidly returned to basal level when elemental diet was replaced by saline. Basal levels of gastric luminal SLI thus showed distinct changes in response to each stimulus. Although the physiological action of luminal SLI remains to be studied, its levels may reflect gastric D-cell activities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296052
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  • 3
    Electronic Resource
    Electronic Resource
    Pancreatic immunoreactive somatostatin and diabetes mellitus (1984)
    Springer
    Digestive diseases and sciences 29 (1984), S. 625-630 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pancreatic secretions were collected during endoscopic retrograde cholangiopancreatography from 15 subjects without pancreatic, biliary, or hepatic diseases, 11 patients with non-insulin-dependent diabetes, and 11 patients with insulin-dependent diabetes. Pancreatic secretion was stimulated by the intravenous administration of one unit of secretin per kilogram of body weight. Immunoreactive somatostatin (IRS) in the pancreatic juice of the nondiabetic subjects ranged from 43 to 97 pg/ml, in non-insulin-dependent diabetics from 5 to 3872, and in the insulin-dependent diabetics from 0 to 2093. IRS in insulin-dependent diabetics under good plasma glucose control ranged from 0 to 281 pg/ml, compared to those under poor control who ranged from 518 to 2093 pg/ml. These results indicate that IRS in pancreatic juice is higher in poorly controlled insulin-dependent diabetics than in well controlled insulin-dependent diabetics and nondiabetics. Whether these changes in IRS are purely secondary phenomena or play some pathogenetic role in the disturbed metabolism of diabetes remains to be proven. The chromatographic profile of IRS in pancreatic juice on both gel filtration and high-performance liquid chromatography has indicated that these IRS moieties represent somatostatin 14 and somatostatin 28.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01347295
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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of somatostatin, or a combination (1992)
    Springer
    Breast cancer research and treatment 21 (1992), S. 181-192 
    Details
    ISSN: 1573-7217
    Keywords: experimental breast cancer ; estrogen independent MXT mammary tumor ; LH-RH agonist ; LH-RH antagonist ; somatostatin analog RC-160
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Female BDF1 mice inoculated with MXT (3.2) estrogen independent mouse mammary carcinoma were treated for three weeks with microcapsules of the luteinizing hormone-releasing hormone (LH-RH) agonist [D-Trp6]LH-RH, the antagonist SB-75, the somatostatin analog RC-160, or combinations. The lack of estrogen dependence of the tumor was proved by bilateral surgical ovariectomy, which had no effect. In two experiments, treatment with 25µg/day doses of each analog alone resulted in a significant inhibition of tumor growth as shown by a 40–53% inhibition of tumor volumes, 38–43% decrease in tumor weights, and histological signs of tumor regression. However, the combination of SB-75 or [D-Trp6]LH-RH with somatostatin analog RC-160 caused greater reduction of tumor volume (68 and 61%) or tumor weights (59 and 56%), than single analogs, and histologically the occurrence of apoptosis and decrease in AgNOR numbers was more pronounced in the groups receiving combination therapy. Specific binding sites for [D-Trp6]LH-RH, EGF, and IGF-I were demonstrated in the tumor membranes. The binding capacity of LH-RH receptors was decreased by treatment with the analogs, the greatest down-regulation being caused by combination therapy. A significant decrease in EGF binding capacity was observed after treatment with the LH-RH analogs, alone or especially in combination with somatostatin analog RC-160. The combination of these analogs also caused a reduction in IGF-I receptors. The finding that LH-RH agonists and antagonists and somatostatin analogs inhibit the growth of estrogen independent mammary tumors, and that combinations are more effective than single analogs, might be of practical importance in human breast cancer therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01975001
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  • 6
    Electronic Resource
    Electronic Resource
    Effect of a cytotoxic analog of LH-RH (T-98) on the growth of estrogendependent MXT mouse mammary cancers: Correlations between growth characteristics and EGF receptor content of tumors (1996)
    Springer
    Breast cancer research and treatment 40 (1996), S. 129-139 
    Details
    ISSN: 1573-7217
    Keywords: experimental breast cancer ; LH-RH agonist ; cytotoxic compounds ; EGF receptors ; organ distribution ; AgNOR ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Female BDF mice bearing estrogen-dependent MXT mouse mammary cancers were treated for 4 weeks with a cytotoxic analog of luteinizing hormone-releasing hormone (LH-RH), T-98 (agonist [D-Lys6]LH-RH linked to glutaryl-2(hydroxymethyl)anthraquinone). The effects of T-98 were compared to those of equimolar amounts of the cytotoxic moiety 2-(hydroxymethyl)anthraquinone hemiglutarate (G-HMAQ) and carrier LH-RH agonist [D-Lys6]LH-RH. Both T-98 and [D-Lys6]LH-RH significantly inhibited the growth of MXT cancers, but G-HMAQ had only a minor non-significant effect. Cytotoxic analog T-98 and the carrier [D-Lys6]LH-RH had similar inhibitory hormonal activities on the pituitary-gonadal axis, but T-98 caused a larger reduction in tumor volume and decreased proliferation characteristics such as mitotic activity and AgNOR numbers in tumor cells to a greater extent than the carrier. Tumor inhibition by T-98, [D-Lys6]LH-RH, and ovariectomy was connected with a significant decrease in binding capacity of EGF receptors in tumor cell membranes. The concentration of EGF receptors remained high in tumors that continued to enlarge in spite of treatment and in all control untreated tumors, even those of small size. Thus, the changes in EGF receptors are likely to be the result of the therapy. Treatment with T-98 caused a greater reduction in the binding capacity of EGF receptors in tumors than [D-Lys6]LH-RH. This could explain the higher inhibitory effect of the cytotoxic analog on tumor growth. Since radiolabeled T-98 was shown to accumulate in MXT cancers 3 hours after a subcutaneous injection, this indicates that specific targeting might play a role in the antitumor effect exerted by this cytotoxic analog.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01806208
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibition of growth of MCF-7 MIII human breast carcinoma in nude mice by treatment with agonists or antagonists of LH-RH (1992)
    Springer
    Breast cancer research and treatment 21 (1992), S. 35-45 
    Details
    ISSN: 1573-7217
    Keywords: LH-RH analogs ; chemical castration ; hormone-independent breast cancer ; nude mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Human breast carcinoma (MCF-7 MIII), which exhibits an estrogen-independent but estrogenresponsive phenotype, was xenografted in 8–9-week-old intact female athymic nude mice without estrogen supplementation. In this model, we investigated inhibitory effects of the modern luteinizing hormonereleasing hormone (LH-RH) antagonist SB-75 and the agonist D-Trp6-LH-RH. The analogs were administered in the form of sustained delivery systems (microcapsules and microgranules). In the first experiment, treatment lasted 10 weeks. After 9 weeks of treatment, a significant inhibition of tumor volume was first found only in the group treated with SB-75, but the final tumor volume was significantly suppressed both by D-Trp6-LH-RH and SB-75. In the second experiment, treatment was started 70 days after tumor transplantation and was continued for 6 weeks. Chronic treatment with SB-75 or D-Trp6-LH-RH appeared to completely arrest tumor growth as measured by tumor volume, percentage change in tumor volume, and tumor weight. Serum estradiol was suppressed to undetectable levels and LH levels were also diminished. Histologically, the regressive changes in the treated tumors were due to the enhancement of apoptosis (programmed cell death) of tumor cells. Membrane receptor assays showed that LH-RH binding sites were down-regulated in tumor cells after treatment with SB-75 or D-Trp6-LH-RH. The results indicate that the antagonist SB-75, released from sustained delivery systems, can inhibit the growth of MCF-7 MIII tumors as effectively as the agonist D-Trp6-LH-RH, but more rapidly. In view of its immediate blockade of the pituitary-gonadal axis and the absence of side effects, the LH-RH antagonist SB-75 might be considered as a possible new hormonal agent for the treatment of breast cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01811962
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