Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report details clinical and pathologic aspects of a patient with small cell undifferentiated carcinoma of the prostate and systemic hyperglucagonemia. A panel of potential serologic markers was evaluated in order to document additional evidence of ectopic hormonal production. Immunocytochemical markers were sought in tissue samples from the primary neoplasm and a lung metastasis. Stains were positive for corticotropin (ACTH) and gastrin in both the prostate and in the lung, but no evidence of excess secretion was documented. These findings are consistent with the notion that neuroendocrine activity is common in undifferentiated small cell carcinomas, regardless of their site of origin.
Cancer 1991 Feb 15
PMID:Small cell carcinoma of the prostate. 184 67

The authors report a patient with ectopic adrenocorticotropic hormone (ACTH) syndrome (EAS) resulting from small cell lung cancer. Treatment with ketoconazole (KCZ) resulted in significant suppression of serum cortisol levels. The authors confirmed KCZ to be a useful adjunct in the treatment of Cushing's syndrome.
Cancer 1991 Mar 01
PMID:The use of ketoconazole in ectopic adrenocorticotropic hormone syndrome. 184 77

In order to investigate the involvement of opioid peptides and prolactin in stress-facilitated mammary cancer, we studied the effect of chronic restraint stress on dimethylbenz[a]-anthracene (DMBA)-induced mammary tumorigenesis and the effect of an opiate antagonist, naltrexone, on this process. Female Fischer-344 rats (n = 160) were administered 15 mg DMBA/ml of sesame oil/rat by intragastric intubation. Eighty rats were subjected to daily 30 min restraint stress in a plastic cylinder, and 80 rats served as control not subjected to the stressor. Half of the rats from each group received naltrexone (1 mg/kg, i.p. daily). Five rats from each group (restraint stress +/- naltrexone and control +/- naltrexone) were killed every 2-3 weeks. Rats subjected to restraint stress developed a greater number of tumors earlier. Naltrexone decreased the tumor incidence in the stressed animals from 32 to 12% (P less than 0.001) and in unstressed rats from 27 to 15% (P less than 0.001) at the end of 18 weeks. Stressed rats showed a decrease of 48% (P less than 0.001) in the level of hypothalamic beta-endorphin. Plasma prolactin increased from 4-13 ng/ml in the control rats to 109-396 ng/ml (P less than 0.001) in the stressed rats throughout the 18 week period. The beneficial effect of naltrexone was associated with 42% (P less than 0.01) increase in T cell proliferation, but greater than 90% (P less than 0.001) decrease in plasma prolactin level was observed in naltrexone-treated rats compared to the untreated animals. Rats subjected to restraint stress showed a 15% (P less than 0.001) decrease in weight gain at the end of the experiment (18 weeks). Neither restraint stress nor naltrexone administration affected the caloric intake of rats during this period. Thus, we believe that restraint stress facilitates DMBA-induced mammary tumors by releasing beta-endorphin and prolactin, and naltrexone shows a beneficial effect by opposing the effect of beta-endorphin on prolactin release in the stressed animals.
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PMID:Facilitation of dimethylbenz[a]anthracene-induced rat mammary tumorigenesis by restraint stress: role of beta-endorphin, prolactin and naltrexone. 190 24

Suramin is a polyanionic compound which has been used in the treatment of trypanosomiasis and acquired immunodeficiency syndrome (AIDS), while preliminary success has been reported in the treatment of cancer. However, suramin also causes adrenal insufficiency. We have previously reported that suramin selectively inhibited corticotropin (ACTH)-stimulated corticosterone release by dispersed adrenal cells in a dose-dependent manner via a direct interaction with the ACTH molecule. The present study was undertaken in order to investigate the effect of suramin on hormone release by dispersed rat anterior pituitary cells. Suramin at a concentration of 100 microM inhibited both basal and secretagogue-stimulated ACTH release by cells cultured in minimal essential medium (MEM) only, while it had no effect on ACTH release by cells cultured in MEM + 10% fetal calf serum (FCS) or MEM + 0.1% bovine serum albumin (BSA). In addition, suramin also caused a parallel decrease of prolactin (PRL) and growth hormone (GH) release by cells cultured in MEM only, suggesting a toxic, rather than a selective effect of suramin on anterior pituitary cells cultured in MEM only. In addition, suramin potentiated the effect of thyrotropin-releasing hormone (TRH) on PRL release by cells cultured in MEM + 10% FCS and suppressed the inhibitory effect of dopamine (DA) on PRL release by cells cultured in MEM + 10% FCS and in MEM + 0.1% BSA. Comparable suppressive effects of suramin on growth hormone-releasing hormone (GHRH)-stimulated and somatostatin (SRIH)-inhibited GH release were found in cells cultured in MEM + 0.1% BSA but not in cells cultured in MEM + 10% FCS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of suramin on hormone release by cultured rat anterior pituitary cells. 198 Aug 98

A histopathologic review of 1985 cases of endometrial carcinoma yielded 31 undifferentiated carcinomas (1.6%). Forty-eight percent were large cell type and 52%, intermediate/small cell type. Twenty-one tumors were examined immunohistochemically. All stained for keratin. Eleven tumors reacted with vimentin antibodies, two with carcinoembryonic antigen antibodies, and ten with neuron-specific enolase (NSE) antibodies (four of which stained for bombesin, two for beta-endorphin, one for prealbumin, five for Leu7, and four for synaptophysin). The mean age at diagnosis was 63.9 years (range, 45 to 86). The crude 5-year and 10-year survival was 58% and 48%, respectively. Seventy-nine percent of the patients in surgicopathologic Stage I and 33% in Stage II survived 5 years. The intermediate/small cell types had a somewhat better prognosis than the large cell type, but the difference was not statistically significant. The presence or absence of NSE and vimentin immunoreactivity had no influence on survival. All patients with tumors infiltrating less than one half of the myometrium survived 5 years in contrast with 46% of the patients with deep infiltrating tumors. Fifty-four percent of the patients with demonstrable vessel invasion survived 5 years in contrast with 89% not so affected.
Cancer 1991 Jul 01
PMID:Undifferentiated carcinoma of the endometrium. A histopathologic and clinical study of 31 cases. 204 61

Several experiments have demonstrated that there is a relationship between neuroendocrine and immune systems. Despite these interesting findings, only few studies have been performed up to now to evaluate the possible importance of neuroimmune interactions in influencing the biological efficacy and toxicity of cancer immunotherapy with IL-2. To analyze the effects of IL-2 on endocrine secretions, we have measured by RIA serum levels of cortisol, beta-endorphin, GH, PRL and of the pineal hormone melatonin in metastatic renal cancer patients, treated with 5-day courses of IL-2 at a daily dose of 3 x 10(6) U/m2, given through a 24-hour intravenous infusion. Six IL-2 courses were evaluated, by collecting blood samples at 4-hour intervals for 24 hours and by comparing the hormonal values with those observed in baseline conditions. Both cortisol and beta-endorphin mean values significantly increased during IL-2 infusion. GH and PRL also increased, but not in a significant manner. Finally, melatonin mean levels significantly decreased during the infusion. The IL-2-induced effects on cortisol, beta-endorphin and melatonin resulted in a complete abolition of their physiological circadian rhythm. These results show that IL-2 infusion induces important changes in endocrine secretions. Because of the immunosuppressive effect of cortisol and the stimulatory one of melatonin, their changes during IL-2 infusion might influence the biological activity of immunotherapy itself. Further studies will be required to define better the clinical importance of IL-2 induced hormonal changes.
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PMID:Endocrine effects of a 24-hour intravenous infusion of interleukin-2 in the immunotherapy of cancer. 214 95

In 66 patients who had to undergo radical abdominal hysterectomy because of cancer of the cervix uteri, the plasma concentrations of beta-endorphin were observed intra- and postoperatively. Two anaesthetic techniques were used: neuroleptanalgesia and thoracolumbar epidural analgesia with sedation and controlled inhalation of a mixture of oxygen and nitrous oxide. While the higher dosage of analgesics administered intraoperatively resulted in markedly lower plasma concentrations of beta-endorphin, there was no such effect in the postoperative phase. Patients with epidural analgesia who were absolutely painless postoperatively had, during that stage, higher concentrations of beta-endorphin in the plasma than those patients who had been given neuroleptanalgesia. They had received no analgetic treatment during the postoperative observation period. These differences are attributed to an increased adaptability of patients subsequent to neuroleptanalgesia. The neuronal block can result in a decrease in functional activity of the suprarenal medulla and impair adaptability. The stress-induced opioid analgesia can be suppressed by circulating enkephalin from the suprarenal medulla.
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PMID:[The quality of analgesia in relation to the plasma concentration of beta-endorphin during neuroleptanalgesia and epidural analgesia]. 214 17

The endocrine action of medroxyprogesterone acetate (MPA) has been claimed to be of a glucocorticoid-like nature. Upon clinical observation, MPA has been shown to improve life quality and overall well-being in patients with advanced breast cancer, renal carcinoma, prostatic carcinoma, and uterine adenocarcinoma. The authors have evaluated MPA endocrine action by the administration of human corticotropin releasing factor (hCRF) in a 90-minute assay in 15 patients with advanced breast cancer or renal cell carcinoma both, before the initiation of oral high-dose MPA treatment (1000 mg MPA) as well as after at least 10 days of therapy. The curves for corticotropin, beta-endorphin, and cortisol responses to hCRF of tumor patients who were tested before the initiation of MPA treatment were parallel to the curves of a healthy control group of probands tested under equal conditions, although at significantly higher respective hormone levels. In patients with malignant disorders assayed after MPA administration, both basal and peak hormone levels were found to be comparable with values obtained in healthy controls. In conclusion, MPA appeared to act at a suprapituitary level since pituitary responsiveness to hCRF was preserved under MPA treatment. Moreover, it appeared that MPA brought the hormonal stress state found in patients with malignant tumors back to normal.
Cancer 1990 Nov 01
PMID:Medroxyprogesterone acetate lowers plasma corticotropin and cortisol but does not suppress anterior pituitary responsiveness to human corticotropin releasing factor. 214 10

Cultured melanoma cells are known targets for the pigment-inducing actions of melanotropins such as alpha-melanocyte-stimulating hormone (alpha-MSH). The objectives of the present studies were to determine the binding properties and functional relevance of MSH binding sites in a mouse melanoma cell line and to determine whether MSH receptors are expressed in situ. The binding properties of MSH receptors in intact cells of a highly metastatic, highly MSH-responsive mouse melanoma cell subline (B16-F10C23) were determined using a radiolabeled, biologically active preparation of the superpotent alpha-MSH analogue, [Nle4,D-Phe7]-alpha-MSH (125I-NDP-MSH). A single high-affinity class of binding site was detected (Kd for NDP-MSH, 5.6 x 10(-11) M; Kd for alpha-MSH, 2.6 x 10(-9) M as determined by Scatchard analysis and heterologous inhibition assays, respectively). alpha-MSH showed nearly identical concentration-response relationships in the radioreceptor assay (inhibition of 125I-NDP-MSH binding) and a bioassay (stimulation of intracellular cyclic AMP accumulation). Furthermore, the respective potencies of three melanotropins, NDP-MSH, alpha-MSH, and adrenocorticotropic hormone, in binding and biological assays were highly correlated. These results indicate that the 125I-NDP-MSH binding site represents the functional MSH receptor. Tumors were induced by inoculation of C57BL/6 mice with B16-F10C23 cells, and the presence of 125I-NDP-MSH binding sites was determined by in situ radiolabeling of frozen tissue sections followed by autoradiography. Specific MSH binding sites were distributed throughout the tumor tissue, but not in associated fibrovascular elements or in neighboring nonmelanoma tissues. As in cultured B16-F10C23 cells, melanotropins inhibited 125I-NDP-MSH binding to tissue sections in a concentration-dependent manner. These results support the hypothesis that functional MSH receptors are expressed in melanoma in situ, suggesting that the activities of melanoma cells in vivo may be subject to modulation by endogenous melanotropins. The methods described will be applicable for studies of the expression and regulation of MSH receptors in human melanoma and other target tissues.
Cancer Res 1990 Feb 15
PMID:Melanotropin receptors of murine melanoma characterized in cultured cells and demonstrated in experimental tumors in situ. 215 54

Ten patients with hepatic metastases from islet cell tumors or carcinoid tumors had clinical symptoms from hormonal secretion and/or pain related to the mass effect of neoplastic liver involvement. Hepatic arterial embolization (HAE) using radiographically guided catheters to inject thrombogenic material was applied to the right and/or left hepatic arteries separately 5 to 7 days apart. All ten patients improved within days of the procedure as confirmed by a decrease in measurable hormone levels (gastrin, adrenocorticotropin, and 5-hydroxy indole acetic acid) or by a decrease in tumor size and improved symptoms. Three patients underwent repeated reembolization from two to four times over nine to 50-month intervals for symptom control. Complications of and indications for HAE in these patients are discussed. It appears to be an effective treatment for dealing with the hormonal syndromes and local symptoms related to the hepatic metastases of hormone-secreting tumors.
Cancer 1990 May 15
PMID:Hepatic arterial embolization for metastatic hormone-secreting tumors. Technique, effectiveness, and complications. 216 Dec 78


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