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)

The control of melanin production, tyrosinase activity, and cell replication by melanocyte-stimulating hormone (MSH) and cyclic AMP (cAMP) was examined in differentially metastasizing B16 mouse melanoma variants. In B16-F1 cells (low metastatic potential), MSH or cAMP greatly elevated tyrosinase activity and melanin content while inhibiting cell replication. The same parameters in B16-F5 cells (intermediate metastatic potential) were altered to a much lesser degree, whereas B16-F10 cells (high metastatic potential) were not significantly affected by MSH or cAMP. Therefore, a correlation exists between loss of hormonal regulation and increased metastatic potential.
J Natl Cancer Inst 1978 Aug
PMID:Control of melanogenesis in mouse melanoma cells of varying metastatic potential. 21 Feb 94

Endocrine and immunohistochemical studies were performed in a patient with lung cancer associated with gynecomastia. Elevated level of human chorionic gonadotropin (hCG) in plasma and mild hyperadrenocorticism were demonstrated by hormone assays. Postmortem examination proved the existence of anaplastic small cell carcinoma of the lung mixed with a feature of chorioepithelioma. The presence of significant amounts of adrenocorticotropic hormone (ACTH), beta-melanocyte stimulating hormone (beta-MSH), calcitonin, gastrin, hCG, hCG-alpha, hCG-beta and human chorionic somatomammotropin (hCS) in tumor tissues was demonstrated by radioimmunoassays, bioassay and immunohistochemical techniques. We present here a unique case of multiple hormones producing tumor elaborating both hormones of amine precursor uptake and decarboxylation (APUD) series (ACTH, beta-MSH, calcitonin and gastrin) and of placental origin (hCG, hCG-alpha, hCG-beta and hCS).
Cancer 1979 Jun
PMID:Multiple-hormone producing lung carcinoma. 22 25

The case of a 38-year-old female with primary argyrophil cell carcinoma of the uterine cervix is reported. Two years after operation the patient developed widespread metastases with typical Cushing's syndrome. Microscopically, the tumor consisted of solid anaplastic cells, adenocarcinoma, and squamous cells. The plasma levels of ACTH and cortisol were elevated. Many cells of both the primary and metastatic tumors showed argyrophilia. Almost all the cells of the metastases contained numerous round secretory granules measuring about 117 micrometers in diameter. Small rod-shaped or larger round secretory granules, measuring 250 and 430 micrometers respectively, were also found in a few of these cells. The tumors in the right lung, pancreas, and kidney contained high levels of ACTH, beta-MSH, serotonin, histamine, and amylase. This is the first report of ectopic production of these five substances from argyrophil cell carcinoma of the uterine cervix.
Cancer 1979 Nov
PMID:Argyrophil cell carcinoma of the uterine cervix with ectopic production of ACTH, beta-MSH, serotonin, histamine, and amylase. 22 79

The pharmacokinetics and the hormonal, analgesic, and behavioral effects of several doses of human beta-endorphin were evaluated after intravenous administration to three patients and intracerebroventricular administration to one patient with pain caused by cancer. These effects were compared to the hormonal effects of intravenously administered morphine sulfate in two patients and an enkephalin analog in two baboons. The mean terminal half-life after intravenous administration of 5 or 10 mg of human beta-endorphin to three patients was 37 min; the mean volume of distribution was 178 ml/kg, and the metabolic clearance rate was 3.2 (ml/min)/kg. The half-life of beta-endorphin in cerebrospinal fluid after intracerebroventricular administration was 93 min, and the volume of distribution was 0.74 ml/kg. A rapid rise in plasma prolactin followed both intravenous and intracerebroventricular beta-endorphin. Intravenous administration did not affect plasma growth hormone, but intracerebroventricular administration suppressed plasma growth hormone. No significant change in plasma growth hormone was noted after intravenous administration of morphine to humans, but plasma growth hormone decreased in one baboon after administration of the enkephalin analog. beta-Endorphin-stimulated release of prolactin occurred at doses lower than those required to produce analgesic and other behavioral effects. When both hormonal and analgesic effects were observed (after 7.5 mg were given intracerebroventricularly), the onset of the hormonal response slightly preceded the analgesic and behavioral responses. These studies suggest that the hormonal effects of beta-endorphin are species dependent and are similar to those of morphine. Hormonal and analgesic effects of beta-endorphin appear to result from the activation of opiate receptors that differ in their locations and characteristics.
 ...
PMID:beta-Endorphin: analgesic and hormonal effects in humans. 29 54

Cells of the C3 clone of B-16 melanoma synthesize melanin only at confluence after which they senesce and can no longer be passaged. Addition to the cultures of 10(-8)--10(-7) M 12-O-tetradecanoylphorbol-13-acetate (TPA) shortly after plating delayed by about 2 days the onset of melanogenesis. TPA did not, however, affect the growth of the cells or the time at which they reached confluence. The ability of a series of phorbol esters to delay melanogenesis correlated with their tumor-promoting activity on mouse skin. The optimum time for addition of TPA was within the first 24 hr after plating; the inhibitory effect decreased when TPA was added at later points. alpha-melanocyte-stimulating hormone (5 x 10(-7) M) added to B-16 cultures 24 hr after plating slowed the growth of the cells and caused them to differentiate when still subconfluent. TPA also inhibited this alpha-melanocyte-stimulating hormone-induced melanogenesis. These results suggest that TPA inhibits a very early stage in a stepwise process that leads to the differentiation of these cultures. For reasons that are not apparent, the cells eventually escape from this inhibition. The B-16 melanoma cell culture system may be useful for studying the mechanism by which TPA and related tumor promoters affect cellular differentiation.
Cancer Res 1979 Oct
PMID:Effect of phorbol ester tumor promoters on the expression of melanogenesis in B-16 melanoma cells. 47 28

Cloudmann S 91 mouse melanoma cells treated for 5 days with melanocyte-stimulating hormone (MSH), cytochalasin B (CB), or both, exhibited changes in cell volume, population, nucleation, and pigment production. Cells treated with CB or CB in combination with MSH were eight to nine times larger, rounder, multinucleated, and heavily pigmented. CB alone increased melanin and DNA per nucleus threefold. CB in combination with MSH increased melanin per nucleus 30-fold. Data on DNA per nucleus suggest that CB-treated cells remained in the G phase longer than did control cells. MSH alone caused a reduction in cell population and a fourfold increase in melanin per nucleus.
J Natl Cancer Inst 1976 May
PMID:Response of Cloudman S91 melanoma cells to melanocytestimulating hormone: enhancement by cytochalasin B. 99 99

Simultaneous elevated levels of ectopic arginine vasopressin (AVP) and ectopic adrenocorticotropin (ACTH) were found in a patient with small cell carcinoma (SCC). The finding of one of these paraendocrine syndromes at the time of diagnosis is common; however, the simultaneous presence of both syndromes has been reported in the literature only on four occasions in the past 25 years. This is the only report in which elevated plasma levels of both hormones are documented in a patient who simultaneously fulfills the criteria for the syndrome associated with each ectopically produced peptide. In the English-language literature, this is the first case that demonstrates by immunohistochemical staining the presence of both of these hormones in the patient's neoplasm. In addition to the use of radiographs, the presence of paraendocrine disorders can provide a method of monitoring the patient's response to therapy. The levels of ACTH and AVP were assayed during this patient's course and correlated with disease refractory to therapy, resulting in poor survival.
Cancer 1992 May 01
PMID:Small cell carcinoma with two paraendocrine syndromes. 131 26

A hybrid toxin targeted to melanotropin receptors and selectively cytotoxic to melanoma cell lines in vitro has recently been developed. The toxin, a recombinant fusion protein (designated DAB389-MSH), contains the peptide sequences of alpha-melanocyte-stimulating hormone (alpha-MSH) and the catalytic (cytotoxic; Fragment A) and lipophilic (part of Fragment B) domains of diphtheria toxin. In the present study, binding of DAB389-MSH to melanotropin receptors in biopsy specimens of human and mouse melanoma metastases was assessed by measuring its ability to inhibit binding of a radiolabeled, superpotent analogue of alpha-MSH (125I-[Nle4,D-Phe7]-alpha-MSH; 125I-NDP-MSH) and comparing its potency in this system with those of the established ligands NDP-MSH and alpha-MSH. Radioligand binding to tissue sections in vitro was localized and quantified by autoradiography and image analysis. DAB389-MSH inhibited binding of 125I-NDP-MSH to experimental murine B16-F1C23 melanoma metastasis tissue and to melanoma metastases of three patients. In both mouse and human melanoma tissues, concentration-response relationships for DAB389-MSH-mediated inhibition of 125I-NDP-MSH binding were parallel, and its maximal effects were comparable in magnitude, to those of NDP-MSH and alpha-MSH. Half-maximal peptide concentrations for inhibition of 125I-NDP-MSH binding to mouse melanoma tissue sections were: NDP-MSH, 0.63 nM; alpha-MSH, 3.14 nM; and DAB389-MSH, 10.1 nM. In human melanoma tissues, the respective half-maximal peptide concentrations for inhibition of 125I-NDP-MSH binding to mouse melanoma tissue sections were: NDP-MSH, 1.80 nM; alpha-MSH, 2.43 nM; and DAB389-MSH, 11.9 nM. Taken together, these results suggest that NDP-MSH, alpha-MSH, and DAB389-MSH bind to a common melanotropin receptor in human metastatic melanoma cells. Since previous work has shown that melanotropin receptors are detectable in melanoma metastases of about 80% of human patients, malignant melanoma cells of many patients may be susceptible to killing by the melanotropin receptor-targeted cytotoxin DAB389-MSH.
Cancer Res 1992 May 01
PMID:Interaction of an alpha-melanocyte-stimulating hormone-diphtheria toxin fusion protein with melanotropin receptors in human melanoma metastases. 131 97

The clinical and laboratory findings in 76 patients with isolated corticotropin deficiency (10 of our own and 66 from literature) were analyzed with the following observations. With the exceptions of hyperpigmentation and hyperkalemia, the similarity of symptoms and signs to those of Addison's disease and their reversibility by glucocorticoids indicate that most, but not all, manifestation of isolated corticotropin deficiency is caused by glucocorticoid deficiency. Isolated corticotropin deficiency seems to be of pituitary origin in most patients, as shown by lack of corticotropin response to insulin-induced hypoglycemia, vasopressin, or corticotropin-releasing factor. Secretion of other pituitary hormones is frequently abnormal, which is mostly attributable to glucocorticoid deficiency. Although the pathogenesis of isolated corticotropin deficiency is unknown in most patients, association with other autoimmune endocrinopathies, postpartum onset in women, or serum antipituitary antibodies suggests an autoimmune pathogenesis in some patients. In two of our 10 patients, cancer developed during glucocorticoid treatment. More observations of complications and long-term prognosis following glucocorticoid therapy are needed for optimal clinical decision making.
 ...
PMID:Isolated corticotropin deficiency in adults. Report of 10 cases and review of literature. 132 48

The differentiation-inducing activity of doxorubicin on B16 melanoma cells grown in vitro was compared with that of other known differentiation inducers, such as theophylline, retinoic acid, and melanocyte-stimulating hormone (MSH). At drug concentrations resulting in cytostatic effects, doxorubicin and theophylline induced morphological changes (dendritic-like structures with a terminal melanin granule) with an enhancement of total melanin content and tyrosinase activity. Retinoic acid did not alter melanin content and cell morphology, although it affected cell growth. MSH enhanced total melanin content and tyrosinase activity, with no significant morphological changes. Flow cytometric analysis showed that MSH led to an accumulation of cells in G1 phase whereas doxorubicin induced an accumulation of cells in G2 + M. Studies on DNA content in doxorubicin-treated cells, selected on the basis of a morphologically differentiated pattern, showed a clustering of these cells in G2 + M, probably due to a cytokinesis block. Thus doxorubicin can induce cell differentiation comparable with other differentiation inducers.
Eur J Cancer 1992
PMID:Comparative studies on the effects of doxorubicin and differentiation inducing agents on B16 melanoma cells. 132 7


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