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)

Interferon causes profound biological changes when given to patients with cancer and many of these could not be predicted from in vitro or animal model systems. We documented significant changes in hormonal levels for a group of 18 patients who were participants in a Phase I gamma-interferon trial. Adrenocorticotropic hormone, cortisol, and growth hormone were all significantly elevated 2 h after treatment with gamma-interferon, with cortisol and adrenocorticotropic hormone returning to base line by 24 h. A placebo group failed to show this change, suggesting a specific interferon effect. Possible mechanisms for these findings and implications for the use of interferons are discussed.
Cancer Res 1987 Dec 01
PMID:Effects of gamma-interferon on the endocrine system: results from a phase I study. 282 31

In an epidemiological study, we evaluated the human amino-terminal portion (IR-hNT) of pro-opiomelanocortin (POMC) as a biomarker for lung cancer by measuring it by radioimmunoassay in the plasma of 180 patients with various histological types of pulmonary carcinoma. Seventy-seven patients with other cancers or benign lung disorders were our controls. An elevated IR-hNT level was measured in 12 percent of the lung neoplasm cases (22% in small-cell carcinoma) and in only 6 percent of the controls. The mean level in the lung cancer group was also higher than in the controls (p = 0.004), while it was higher in patients with small-cell carcinoma than in those with squamous-cell and adenocarcinoma (p = 0.013 and 0.002, respectively). Otherwise, we demonstrated a correlation between IR-hNT levels and altered liver function only in patients with a lung malignancy (p varying between 0.015 and less than 0.001). Finally, survival analysis failed to show that IR-hNT has a prognostic value when measured at the onset of lung cancer. These results allow us to conclude that IR-hNT, although not very sensitive in screening for carcinoma of the lung, may indicate the presence of liver metastases in this disease.
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PMID:The role of the NH2-terminal portion of pro-opiomelanocortin as a biomarker for human lung cancer. 282 12

Receptor binding studies demonstrated specific high-affinity, saturable binding of a number of opioid ligands to a wide variety of neural and nonneural human and animal tumors. Radioimmunoassays revealed the presence of beta-endorphin and methionine-enkephalin in these tumors. Both methionine- and leucine-enkephalin were detected in tumor tissue by immunocytochemistry, with immunoreactivity related to the cortical cytoplasm of tumor cells, but not to cell nuclei. Endogenous opioids and receptors were found in benign and malignant tumors representative of ectodermal, mesodermal, and endodermal origin. Receptors and endogenous opioid peptides were present in tumors from many different species, including those transplanted into nude mice. These results suggest that opioid receptors and endogenous opioids are fundamental features of human and animal cancers.
J Natl Cancer Inst 1987 Nov
PMID:Opioid receptors and endogenous opioids in diverse human and animal cancers. 282 13

It has been previously reported that sauna-induced fevers (approximately 39 degrees C) result in rises of beta-endorphins in normal volunteers. This report describes changes in plasma beta-endorphins in cancer patients undergoing whole body hyperthermia (40.5 degrees C to 41.8 degrees C). Results presented show that there is a linear relationship between thermal stress, defined in terms of core temperature and/or duration of hyperthermia, and the quantitative rise in plasma beta-endorphin levels. Data relating to changes in ACTH and cortisol levels are in a single temperature range (41.5 degrees C--41.8 degrees C) are also reported.
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PMID:Rise in plasma beta-endorphin, ACTH, and cortisol in cancer patients undergoing whole body hyperthermia. 282 24

The presence of alpha-MSH receptors on human melanoma has so far been suggested in the literature but not proved. We describe a reproducible and specific binding assay of alpha-MSH on human melanoma cells, using a high-specific-activity 125I-labelled hormone (1.5 to 2 mCi/micrograms) with consistent receptor binding (usually exceeding 2 pg/10(6) cells) and stable for 3 weeks. Asynchronized cells in suspension were incubated for 15 min at 37 degrees C with the tracer and various concentrations of unlabelled hormones. Synthetic alpha-MSH was compared to beta-MSH, ACTH1-24, ACTH4-10, beta-LPH, CLIP, CRF, MIF I, A8VP and beta-endorphin. Out of a panel of 8 human melanoma cell lines, 3 showed specific and reproducible alpha-MSH binding curves. No significant binding to human fibroblast and human carcinoma cells was seen. alpha-MSH, beta-MSH and, to a lesser extent ACTH4-10 (a part of the alpha-MSH sequence) were the only peptides able to displace labelled alpha-MSH from its binding sites, indicating the high specificity of the MSH receptor. Affinity constants (Ka) ranged from 10(8) to 10(9) l/mole and the estimated receptor number was 1,000 to 2,000 per cell. We conclude that some human melanoma cell lines expressed specific MSH receptors with stable affinity but which are low in number.
Int J Cancer 1988 Feb 15
PMID:Evidence for alpha-melanocyte-stimulating hormone (alpha-MSH) receptors on human malignant melanoma cells. 282 46

The melanocytotoxic effects of 4-hydroxyanisole (4-OHA) are thought to depend upon its conversion to toxic oxidation products by the enzyme tyrosinase. In this study, the cytotoxicity of 4-OHA was examined in different B16 melanoma cell lines that show varying levels of tyrosinase and after stimulation by melanocyte-stimulating hormone (MSH) and all-trans-retinoic acid (RA). 4-OHA decreased cell survival of three melanotic and one amelanotic cell line in culture, but the effect was unrelated to their tyrosinase activity or the subcellular localization of the enzyme. Although stimulation of tyrosinase activity with RA enhanced the cytotoxicity of 4-OHA, no similar enhancement occurred with alpha-MSH. It appears that there is no relationship between the cytotoxic effects of 4-OHA and intracellular tyrosinase and the enhancement of its cytotoxicity by RA may well be related to the antiproliferative effects of the retinoid.
Eur J Cancer Clin Oncol 1988 Dec
PMID:Cytotoxicity of 4-hydroxyanisole and tyrosinase activity in variant cell lines of B16 melanoma. 285 44

Mammary tumors were induced in female Sprague-Dawley rats by giving a single oral dose of 20 mg 7,12-dimethylbenz[a]anthracene (DMBA). Animals were killed after full development of tumors 4 months after the ingestion of DMBA. Opioid peptides in various tissues were estimated by radioimmunoassay (RIA). Tumor-bearing rats (n = 5) had higher (P less than 0.05) contents of beta-endorphin in pituitary (+60%), striatum (+52%) and midbrain (+85%) compared to animals with no tumors. However, tumor-bearing rats showed a decrease of 35% in striatal met-enkephalin content. Dynorphin level decreased (P less than 0.05) in pituitary (-49%) and hypothalamus (-29%) of tumor-bearing rats. Thus for the first time, we report the alteration in the level of these neuropeptides during the process of chemical carcinogenesis.
Cancer Lett 1986 May
PMID:Effect of 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis on the opioid peptide levels in the rat central nervous system. 287 Jul 95

Using the "Bi-Digital O-Ring Test Molecular Identification and Localization Method," one can identify and localize minute amounts of bioactive substances (including neurotransmitters), micro-organisms, toxic substances, or drugs, and, in addition, one can non-invasively image normal organs as well as screen for and image the distribution of specific types of cancer of specific internal organs without using any expensive instrumentation. One can also use this method to perform a qualitative analysis of neurotransmitters, neuromodulators, and hormones on different parts of the imaged organs. The molecule or substance being investigated is compared with a minute amount of a pure control reference substance, and if the substance identical to the control reference substance exists, then the electro-magnetic waves emitted by the identical substance will produce an electro-magnetic resonance phenomenon with the electro-magnetic waves of identical resonance frequency emitted by the control reference substance, and this resonance phenomenon is hypothesized to be the basis of the "Bi-Digital O-Ring Test Molecular Identification and Localization Method." The following substances have been used as control reference substances to identify and localize identical substances in vitro and in vivo: pure neurotransmitters (e.g. serotonin, beta-endorphin, methionine-enkephalin, norepinephrine, dopamine, L-dopa, substance P, etc.), as well as L-tryptophan and L-tyrosine; cholesterol; steroid hormones (including aldosterone, corticosterone, cortisol, progesterone, testosterone, etc.); peptide hormones; microscopic slides of normal organs; microscopic slides of specific cancer cells of specific organs (e.g. adenocarcinoma of the head of the pancreas, adenocarcinoma of the descending colon, etc.); microscopic slides of pure micro-organisms; toxic substances (e.g. lead, mercury, KCN); drugs (including non-steroidal anti-inflammatory drugs, antibiotics, beta-blockers, calcium channel blockers, etc.); and antibodies against specific substances or micro-organisms. An intensive network of serotonin and L-tryptophan was discovered, by using the "Bi-Digital O-Ring Test Molecular Identification and Localization Method," in different parts of the body. In general, in painful areas, frequently serotonin is markedly reduced, L-tryptophan is markedly increased, and substance P is markedly increased, while in non-painful areas, serotonin is markedly increased, L-tryptophan is markedly decreased, and substance P is markedly decreased.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:"Bi-digital o-ring test molecular identification and localization method" and its application in imaging of internal organs and malignant tumors as well as identification and localization of neurotransmitters and micro-organisms--Part 1. 287 19

MTC is characterized by multiple humoral and hormonal manifestations. Although calcitonin is the specific marker of the disease, somatostatin, the pro-opiomelanocortin derived peptides and bombesin--among hormones produced by the tumor--can represent an exacerbation of normal C cells potentialities through genome derepression induced by the cancer. In this paper, the functional polymorphism of princeps tumoral markers and the endocrinological aspects of this neoplasia are reviewed. Molecular biology has been instrumental in discovering new tumoral peptides ("ancestral" CT forms, cryptic peptide and CGRP) and methods of CT detection; therefore, the role of CT could be better evaluated. In addition to its calciotropic role, CT acts also as a neuromodulator on some hypophyseal hormones. Conversely, CT secretion is also regulated by amines and neuropeptides, providing the basis of potential hormonal treatment.
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PMID:[Tumor markers of medullary cancer of the thyroid body. Basic and endocrine aspects]. 290 Jun 20

There has been considerable effort in chemically conjugating a variety of plant and bacterial toxins to monoclonal antibodies that are directed to surface antigens on target cells. Coupling has been mediated through disulfide linkage, and the resulting conjugates are known generically as immunotoxins. In general, there are a few shortfalls to this approach. For example, since it is clear that not all surface antigens are internalized, one cannot predict the fate of a given IT once bound to its determinant on the surface of a target cell. In addition, in most instances one must activate the amino moiety of lysine residues with a heterobifunctional reagent in order to form disulfide linkage between the ligand and toxophore components. Since the number of reactive groups may be large, the disulfide linked conjugate molecules most likely represent a family of isomeric molecules rather than a defined protein. As a result, one cannot readily manipulate the fine structure of an IT in order to probe the mechanism of toxophore entry into the target cell. The approach that our group has taken toward the development of targeted cytotoxins, however, differs in a fundamental way: Rather than chemically coupling the ligand with toxophore through a disulfide bond, we have turned to genetic engineering in order to create gene fusions whose chimeric products are joined through a peptide bond. Thus, we have genetically constructed a family of fusion genes in which the receptor binding domain of diphtheria toxin has been deleted and replaced with DNAs encoding either alpha-MSH or IL-2. In each instance, it was known that the polypeptide ligand component of the fusion protein bound to specific receptors on target cells and was internalized by receptor mediated endocytosis. We reasoned, therefore, that the substitution of the diphtheria toxin receptor binding domain by these ligands should result in the formation of 'new' toxins whose action should be targeted toward selected eukaryotic cells that expressed either the alpha-MSH or IL-2 receptor. As along as the ligand component was exposed on the surface of the chimeric toxin, the molecule should bind to its receptor and be drawn into the cell by receptor-mediated endocytosis. Since the toxin-related/peptide hormone fusion protein is the product of a chimeric gene, it is a single molecular species. This has allowed us to begin to probe by site-directed mutagenesis the structure of fragment B sequences that are required to facilitate the translocation of fragment A across the target cell membrane.(ABSTRACT TRUNCATED AT 400 WORDS)
Cancer Treat Res 1988
PMID:Diphtheria-related peptide hormone gene fusions: a molecular genetic approach to chimeric toxin development. 290 22


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