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)

Circulating osteocalcin (OC) and cortisol levels were measured in blood samples from 93 patients with dissaminated prostate cancer. Among these subjects 79 had not responded to therapy, while 14 had responded to a variety of anticancer treatment strategies (orchiectomy, cyproterone acetate (CPA), flutamide, Buserelin, diethylstilbestrol (DES), Estracyt, and polyestradiol phosphate). The control group consisted of 19 patients with benign prostatic hypertrophy. In the majority of these patients blood adrenocorticotropic hormone (ACTH), estradiol human growth hormone (hGH), and thyroid stimulating hormone (TSH) levels were also assessed. In nonresponders to therapy with DES and Estracyt subnormal circulating OC levels were measured, while normal OC values were found in nonresponders to other treatment strategies. In patient given Estracyt highly elevated estradiol levels were recorded. Subnormal and/or low-normal estradiol concentrations were found in patients subjected to CPA and DES. Elevated blood cortisol levels were assessed in subjects treated with DES and Estracyt while at the same time either subnormal and low-normal plasma ACTH concentrations were measured in these same patients. Accordingly, the decline observed in OC concentration seems to be a consequence of the well-established inhibitory effect of glucorticoids on osteoblast activity. The decline in blood cortisol levels obtained after administration of dexamethasone in patients given DES and Estracyt may be attributed both to possible changes in catabolic pathways and to the contribution of the negative neuroendocrinological feedback.
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PMID:Plasma osteocalcin values and related hormonal parameters in patients subjected to a variety of prostate anticancer agents. 185 47

Basal levels and adrenocorticotropic hormone (ACTH)-induced increments (delta-values) of serum cortisol, dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), 4-androstene-3, 17-dione (A4), and 17-hydroxyprogesterone (170HP); basal testosterone (T), luteinizing hormone (LH), serum ASAT, gamma-GT, and albumin were measured in prostatic cancer patients before and after 6 months of treatment with LH-RH-agonist, with flutamide, and with LH-RH-agonist + flutamide, respectively. Basal DHA and DHAS were decreased during flutamide and LH-RH-agonist + flutamide treatment and basal A4 during treatment with LH-RH-agonist and with LH-RH-agonist + flutamide. Basal 170HP, T, and LH decreased during LH-RH-agonist and LH-RH-agonist + flutamide treatment and increased during single drug flutamide treatment. Slightly decreased delta cortisol values were observed during LH-RH-agonist and during flutamide treatment and slightly increased delta 170HP values during LH-RH-agonist and LH-RH-agonist + flutamide treatment. Values for delta DHA and delta A4 were completely unaffected by any of the treatment regimens. Elevated ASAT values were observed during treatment with flutamide and with LH-RH-agonist + flutamide. It is concluded that flutamide has no effect on the adrenal androgen response to acute ACTH stimulation.
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PMID:Flutamide has no effect on adrenal androgen response to acute ACTH stimulation in patients with prostatic cancer. 197 1

The xenograft line, UCRU-PR-2, has been characterized further. Established from a primary human undifferentiated small cell carcinoma of the prostate, it has been maintained as a stable xenograft line in nude mice and is currently in passage 9. The tumor has maintained the features of small cell undifferentiated carcinoma but shows epithelial as well as neuroendocrine characteristics. In this paper, we describe synthesis and secretion of peptide hormones, ACTH, beta-endorphin and somatostatin in vivo and ACTH and beta-endorphin in vitro by the tumor, UCRU-PR-2. This suggests that the gene for proopiomelanocortin is expressed and that processing of the molecule occurs. This line may yield insights into the histogenesis of the subtypes of prostate cancer, and also aid studies of regulation of ectopic hormone production.
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PMID:Ectopic hormone production by a prostatic small cell carcinoma xenograft line. 283 15

The last few years have seen the isolation, characterization and synthesis of two new hypothalamic peptides, the growth-hormone releasing factor (GRF) and the corticotrophin-releasing factor (CRF). GRF selectively stimulates pituitary growth hormone. It is interesting to note that GRF was isolated from two pancreatic tumors which were responsible for an acromegalic condition in the two patients. Hypothalamic GRF (1-44) has been found to be identical to this pancreatic GRF. CRF was isolated first from ovine hypothalamus and later characterized in several species and in the human. CRF specifically stimulates the secretion of ACTH and of beta-endorphins, and other fragments of the common precursor named pro-opiomelanocortin. Chemical synthesis of analogues of hypothalamic peptides, and in particular of GnRH (gonadotrophin-releasing hormone), has made available new molecules which form agonists as well as antagonists. After a short period of gonadotrophin stimulation GnRH agonists induce desensitization of the pituitary and a decrease in secretion of the gonadotrophins and the sex steroids by the gonads. Their usefulness is presently being tested in several conditions such as prostate cancer, endometriosis, breast cancer and idiopathic precocious puberty, and as a contraceptive method. On the other hand, pulsatile administration of GnRH restores deficient reproductive functions in certain conditions such as anovulation or azoospermia.
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PMID:[Hypothalamic factors: current findings]. 300 38

A radioimmunoassay procedure for plasma 11-deoxycortisol (S) was developed using an antiserum prepared by immunizing rabbits with S-21-hemisuccinate bovine serum albumin and S-3-oxime-bovine serum albumin. Thereafter plasma S, cortisol (F) and adrenocorticotropic hormone (ACTH) responses to metyrapone were investigated in 13 normal adult males and 39 patients with prostatic cancer. The results were as follows: 1) The antiserum against S-3-oxime-bovine serum albumin had less cross reactivity (less than 10%) with other steroids than that against S-21-hemisuccinate bovine serum albumin and obtained a good standard curve. The intra-assay variance and interassay variance of this method using the former antiserum (N = 10) were 12.4% asd 14.9% respectively, and the blank value was 3.7 +/- 1.6 pg. 2) Basal levels of S. F and ACTH in plasma from 13 normal adult males, ranged 21 approximately 80 years, old, were 98.4 +/- 15.7 ng/dl (mean value +/- S.E.), 12.7 +/- 0.78 micrograms/dl and 30.6 +/- 3.02 pg/ml respectively. Those level increased to 7060 +/- 598 ng/dl, 24.3 +/- 1.69 micrograms/dl and 24.3 +/- 1.6 pg/ml at 9 a.m. following oral administration of metyrapone (30 mg/kg b.w.) at midnight. 3) Both basal levels and responses of plasma S and F to metyrapone increased remarkably, while those of ACTH were within the normal range in prostatic cancer patients during the estrogen therapy. It was considered that protein-bound S and F increased following elevation of corticosteroid binding globulin but returned to the normal range about 2 weeks after discontinuation of the therapy. 4) In case treated wih estrogens, plasma, S, F and AC normal range in prostatic cancer patients during the estrogen therapy. It was considered that protein-bound S and F increased following elevation of corticosteroid binding globulin but returned to the normal range about 2 weeks after discontinuation of the therapy. 4) In case treated wih estrogens, plasma, S, F and AC normal range in prostatic cancer patients during the estrogen therapy. It was considered that protein-bound S and F increased following elevation of corticosteroid binding globulin but returned to the normal range about 2 weeks after discontinuation of the therapy. 4) In case treated wih estrogens, plasma, S, F and ACTH responses to metyrapone were unchanged compared to normal adult males 2 approximately 4 weeks after discontinuation of the therapy, and this data suggested that estrogens had no inhibitory effect on the pituitary-adrenal axis. However, in cases treated with progestational agents over a long-term period, plasma S and ACTH responses to metyrapone decreased slightly but returned to the normal range 2 approximately 4 weeks after discontinuation of the therapy. This suggested that the inhibitory effect of these agents on the pituitary-adrenal axis was mild and reversible.
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PMID:[Plasma 11-deoxycortisol response to single dose metyrapone in prostatic cancer patients (author's transl)]. 626 18

The nonsteroidal androgen-receptor antagonist nilutamide has previously been shown to inhibit adrenal androgen steroidogenesis in patients with prostatic carcinoma treated in combination with an LHRH agonist. In order to understand better the mechanisms subserving this observation, we have studied the effects of nilutamide alone on the serum concentrations of androstenedione (A), dehydroepiandrosterone (DHEA), and DHEA-sulphate (DHEA-S) in 12 patients with prostatic cancer and compared them with those achieved in 21 patients treated with the agonist D-Trp-6-LHRH. In addition, the adrenocorticotropic hormone (ACTH)-stimulated adrenal response and the thyrotropin releasing hormone (TRH)-stimulated prolactin (PRL) response observed in the patients treated with nilutamide were compared with a control group of healthy age-matched controls. No significant variation in the basal concentrations of adrenal androgens occurred either within or between both treatment groups. In response to ACTH, a decreased 17-alpha hydroxyprogesterone (17-OHP) accumulation and an augmented A/17-OHP ratio were observed in the antiandrogen group (P < 0.05 for both), suggesting the partial removal of the 17,20 lyase block which was distinctive of the untreated controls, while no significant difference was found for other steroids. Basal PRL levels were not affected by the antiandrogen, but the response to TRH was increased. We conclude that no significant inhibition of adrenal androgen secretion occurs after nilutamide or LHRH agonist treatment. Rather, administration of the antiandrogen alone may partially remove the physiological decrease in adrenal androgen secretion observed in the elderly.
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PMID:Effect of the nonsteroidal antiandrogen nilutamide on adrenal androgen secretion. 829 Mar 86

A 57-year-old man showed high serum cortisol, plasma adrenocorticotropin (ACTH) and corticotropin-releasing hormone (CRH) levels with a large pituitary tumor and a prostatic cancer. High dose dexamethasone did not suppress cortisol secretion and CRH administration did not stimulate cortisol secretion. After surgical removal of the pituitary tumor, plasma CRH, ACTH and serum cortisol levels were normalized. Histological examinations showed pituitary adenoma and prostatic adenocarcinoma, and pituitary adenoma was stained with both anti-CRH and anti-ACTH antibodies, but prostatic cancer was not stained. A CRH-producing pituitary adenoma is a new type of Cushing's syndrome.
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PMID:Cushing's syndrome with a large pituitary adenoma producing both corticotropin-releasing hormone (CRH) and adrenocorticotropin (ACTH). 1213 23

Bilateral orchidectomy (ORX) or administration of luteinizing hormone releasing hormone agonist (LHRH) for prostatic cancer patients causes suppression of testicular androgens. However, the suppression of adrenal androgens by these treatments is controversial. We measured serum concentrations of testosterone (T), 4-androstene-3, 17-dione (A-dione), dehydroepiandrosterone (DHEA), LH, follicle-stimulating hormone (FSH), adrenocorticotropic hormone (ACTH) and cortisol before and after 3-12 months of the first hormonal treatment in 17 prostatic cancer patients who had received ORX (8 cases) or LHRH (9 cases). ORX and LHRH decreased serum T to the castration level significantly (ORX: p < 0.001, LHRH: p < 0.0001). ORX increased serum LH and FSH significantly (LH: p < 0.001, FSH: p < 0.001), whereas LHRH decreased LH and FSH significantly (LH: p < 0.05, FSH: p < 0.05). Neither treatment caused any significant change in ACTH or cortisol. ORX and LHRH decreased the serum A-dione significantly (ORX: p < 0.01, LHRH: p < 0.001). LHRH decreased the serum DHEA significantly (p < 0.01), whereas ORX did not decrease serum DHEA. These data suggest that "medical" and "surgical" castration, especially LHRH agonist, may decrease not only testicular androgens but also adrenal androgens.
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PMID:[Change of serum adrenal androgens in prostatic cancer patients after bilateral orchidectomy or LHRH agonist treatment]. 1459 89

This review documents the remarkable progress over the last 50 years of our knowledge of the control of anterior pituitary hormone release and synthesis by a family of peptidic releasing and inhibiting hormones, synthesized in hypothalamic neurons and released into the hypophysial portal vessels. These vessels transport them to the anterior pituitary, where they stimulate release and synthesis of pituitary hormones or inhibit these processes. In general, there are at least two hypothalamic hormones for each pituitary hormone-vasopressin and corticotrophin-releasing hormone (CRH) for adrenocorticotropin hormone (ACTH) and growth hormone-releasing hormone (GHRH) and growth hormone-inhibiting hormone (GIH) for growth hormone (GH). Some of these hormones have extrapituitary action: for example, luteinizing hormone-releasing hormone (LHRH) stimulates mating behavior. High doses of LHRH have an inhibitory action on the growth of prostate cancer. Proinflammatory and anti-inflammatory cytokines act not only in the brain, but also on the pituitary and peripheral tissues. All of these transmitters are controlled by neuronal transmitters. We anticipate further rapid progress and clinical application of these transmitters and the discovery of new ones.
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PMID:Chronology of advances in neuroendocrine immunomodulation. 1719 52

Anorexia and weight loss are part of the wasting syndrome of late-stage cancer, are a major cause of morbidity and mortality in cancer, and are thought to be cytokine mediated. Macrophage inhibitory cytokine-1 (MIC-1) is produced by many cancers. Examination of sera from individuals with advanced prostate cancer showed a direct relationship between MIC-1 abundance and cancer-associated weight loss. In mice with xenografted prostate tumors, elevated MIC-1 levels were also associated with marked weight, fat and lean tissue loss that was mediated by decreased food intake and was reversed by administration of antibody to MIC-1. Additionally, normal mice given systemic MIC-1 and transgenic mice overexpressing MIC-1 showed hypophagia and reduced body weight. MIC-1 mediates its effects by central mechanisms that implicate the hypothalamic transforming growth factor-beta receptor II, extracellular signal-regulated kinases 1 and 2, signal transducer and activator of transcription-3, neuropeptide Y and pro-opiomelanocortin. Thus, MIC-1 is a newly defined central regulator of appetite and a potential target for the treatment of both cancer anorexia and weight loss, as well as of obesity.
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PMID:Tumor-induced anorexia and weight loss are mediated by the TGF-beta superfamily cytokine MIC-1. 1798 62


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