Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrical stimulation of the periaqueductal gray of the rat's midbrain analgesia leads to an increase in the number of artificial pulmonary metastases from the Walker 256 tumor. In an effort to investigate the influence of the pain suppression system and its associated peptides on this phenomenon, we activated the pain suppression system directly from the Nucleus of the Raphe Magnus, a non-opioid subsystem. After inducing analgesia by direct injection of beta-endorphin on the Nucleus of the Raphe Magnus, we noted an increase in the number of artificial pulmonary metastases. This result could be blocked by pretreatment with naloxone. If the Nucleus of the Raphe Magnus was activated by electrical stimulation sufficient to induce analgesia, the metastatic effect was still present but markedly attenuated.
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PMID:Beta-endorphin injected into the nucleus of the raphe magnus facilitates metastatic tumor growth. 608

A 28 year old white women was found to have a cervical tumor in the 25th week of pregnancy. Pathologic examination revealed a nonkeratinizing small cell carcinoma. After delivery by cesarean section, pelvic lymph node exploration was carried out, and all 15 nodes were free of tumor. Her condition was staged as II-A, and she was treated with local radiation. Metastatic disease became manifest almost a year later and was histologically similar to her primary disease. A Cushingoid appearance was noticed and plasma cortisol levels were elevated. Twenty-four hour urinary 17-hydroxycorticosteroid (17-OHCS) and 17-ketosteroid (17-KS) levels were elevated and failed to suppress with dexamethasone. Plasma adrenocorticotropin (ACTH) level was elevated. Electron microscopic examination of the tumor tissue revealed neurosecretory granules. Immunoperoxidase stains for ACTH were positive. The patient's course was one of progressive decline and eventual death. A literature review revealed two other cases in which carcinoma of the uterine cervix was considered to be the source of ectopic ACTH. Some small cell carcinomas of the cervix may arise from cells of the APUD series. Small cell carcinoma of the uterine cervix may behave differently from the more commonly encountered keratinizing and large cell nonkeratinizing carcinomas of the cervix and may not respond as well to standard therapy. Ectopic hormone production, production of abnormal peptides or of vasoactive amines may be more common in small cell carcinoma of the cervix than is currently recognized, and these products may be clinically useful as tumor markers.
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PMID:Cushing's syndrome with small cell carcinoma of the uterine cervix. 610 40

Eighty-one primary ovarian carcinoids and intraovarian metastases from six mid-gut carcinoids were examined for the presence of tumor cells immunoreactive with antisera raised against various neurohormonal peptides, mostly of gastroenteropancreatic (GEP) origin. Twenty of the primary and two of the metastatic carcinoids contained such tumor cells. The incidence of tumors with any kind of neurohormonal peptide immunoreactive tumor cells was 53% in the trabecular carcinoids, and 42% in the strumal carcinoids, whereas the incidence was much lower (7%) in the insular type. Immunoreactive pancreatic polypeptide (PP), glucagon, enkephalin, and somatostatin were those neurohormonal peptides most commonly observed in the tumor cells of the primary carcinoids. Those less commonly found were substance P, calcitonin, VIP, neurotensin, beta-endorphin, and ACTH. Four metastatic carcinoids were nonreactive with all the antisera used. Cells storing immunoreactive insulin, glucagon, PP, VIP, gastrin, substance P, or enkephalin were found in one of the two remaining metastatic carcinoids; in the other only gastrin-immunoreactive tumor cells were observed. The occurrence and distribution of tumor cells storing the neurohormonal peptides in ovarian carcinoids are discussed in relation to their possible origin in the ovary and to carcinoids in the gut.
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PMID:Neurohormonal peptides in ovarian carcinoids: an immunohistochemical study of 81 primary carcinoids and of intraovarian metastases from six mid-gut carcinoids. 611 50

The effects of neuroadenolysis on plasma titres of beta-endorphin, beta-lipotropin, ACTH, TSH and prolactin have been investigated in five patients with metastatic cancer who responded to the treatment and have been in remission for more than four years and in five others who were undergoing the treatment for the first time for pain due to cancer metastases. beta-Endorphin, beta-lipotropin and ACTH titres were within the normal ranges of values in both categories of patients but post-neuroadenolysis titres of these peptides were higher than those before the treatment. The ability to secrete TSH and prolactin and to respond to thyroid stimulating hormone releasing hormone (TRH) remains intact following the treatment. However, whereas basal TSH titres and response to TRH was lower in the majority of patients, no such effect was observed on prolactin secretion. Plasma titres of prolactin and TSH were below the sensitivity of the method in the five patients who are in remission for more than four years. These preliminary findings suggest that neuroadenolysis probably affects some mechanism(s) associated with the control of beta-endorphin, beta-lipotropin and ACTH synthesis.
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PMID:Some aspects of pituitary function after neuroadenolysis in patients with metastatic cancer. 627 71

beta-Endorphin immunoactivity was measured in the plasma and cerebrospinal fluid (CSF) of 13 patients with metastatic cancer 1 day before and 5 days after complete transsphenoidal hypophysectomy. Preoperatively, mean beta-endorphin-like immunoactivity in plasma was 18.2 +/- 3.5 pg/ml (SEM) and in CSF 32.3 +/- 6.3 pg/ml. No correlation was noted between the concentration of beta-endorphin in plasma and CSF. Postoperatively, plasma beta-endorphin was undetectable (less than 7 pg/ml) in 12 patients and was low (9.6 pg/ml) in 1 patient. In CSF, however, beta-endorphin was detectable in 10 of the 13 patients postoperatively, with a mean of 14.0 +/- 2.2 pg/ml. Chromatography on Sephadex G-50 of CSF extracts pooled from 3 patients after hypophysectomy showed that the majority of beta-endorphin immunoactivity eluted in the same position as synthetic human beta-endorphin. We conclude that beta-endorphin becomes undetectable in plasma after hypophysectomy in patients receiving exogenous glucocorticoid replacement but remains detectable in significant amounts in CSF. It appears, therefore, that a considerable portion of the beta-endorphin in CSF is of nonpituitary origin, most likely resulting from synthesis and secretion of this peptide by brain directly into the CSF.
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PMID:Persistence of beta-endorphin in human cerebrospinal fluid after hypophysectomy. 630 34

We report the history, laboratory findings, and studies performed on a 27-yr-old patient with a metastatic parasellar adenoma of the pituitary and Cushing's syndrome. She developed intense hyperpigmentation and extraordinarily high ACTH levels after bilateral adrenalectomy in 1974. With the exception of marked hyperpigmentation, she did well on glucocorticoid replacement therapy until August 1979, when multiple hepatic nodules were observed during a cholecystectomy. Histological studies and immunoperoxidase staining indicated that these lesions were pituitary tumor metastases. What were presumed to be metastatic lesions also developed in lungs and bone. This combination of liver, bone, and lung metastases from primary pituitary tumors has not previously been reported. Immunoreactive plasma ACTH concentrations were as high as 230,000 pg/ml. Similarly, high levels of plasma immunoreactive beta MSH and immunoreactive beta-endorphin were found. High doses of glucocorticoids reduced the concentration of ACTH to one seventh to one tenth the basal level. The sensitivity of plasma ACTH to exogenous steroid administration strongly suggests that an intact intracellular mechanism for negative feedback control of ACTH secretion persisted within the tumor cells. The rapid rise in ACTH and related peptides and the development of metastases after adrenalectomy suggest that both the secretory capacity and the oncogenic potential of the parasellar tumor were chronically inhibited by glucocorticoid hormones.
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PMID:A pituitary parasellar tumor with extracranial metastases and high, partially suppressible levels of adrenocorticotropin and related peptides. 630 34

Metastasis is a complex process whereby tumour cells from a primary neoplastic growth disseminate throughout the body and establish secondary tumour foci in distant organs. Biochemical traits associated with, or essential for, the expression of the metastatic phenotype have not yet been identified. In the course of examining stimulation of the B16 murine melanoma adenylate cyclase by melanocyte-stimulating hormone (MSH) and by the diterpene forskolin, we noted that tumour cell clones isolated from common parent cell populations differed widely in their responses to these agonists. We report here that the accumulation of cyclic AMP induced by MSH or forskolin shows a strong positive correlation with the ability of B16 melanoma clones to form pulmonary tumour colonies when injected intravenously (i.v.) into syngeneic mice ('experimental metastasis'). In parallel in vitro analyses of cyclic AMP metabolism and in vivo assays of experimental metastasis using replicate cell preparations, highly metastatic tumour cell clones consistently show greater than a 30-fold increase in cellular cyclic AMP when exposed to MSH or forskolin. By contrast, clones with limited metastatic abilities respond to the same agonists with only a two- to threefold increase in cellular cyclic AMP. These data suggest that cyclic AMP metabolism is linked with biochemical pathways that are responsible for the formation of experimental metastasis by the B16 melanoma.
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PMID:Experimental metastasis correlates with cyclic AMP accumulation in B16 melanoma clones. 632 99

A 36 year old woman with hypercorticism and markedly elevated blood ACTH levels underwent pituitary ablation because of suspected hypophysial Cushing's disease. Since no adenoma was detected in the anterior lobe and the hypercorticism persisted, a bilateral adrenalectomy was performed. Four months later lymph node and mediastinal metastases of an anaplastic small cell carcinoma, with the presence of argyrophil granulation, as well as immunoreactive 19-39ACTH, beta-LPH and alpha-endorphin, were found. The primary site of ectopic ACTH production was not revealed. A light and electron microscopic study of the adrenals, in addition to cortical hyperplasia, disclosed numerous small cells associated with nonmyelinated sympathetic nerve fibers and containing cytoplasmic inclusions indistinguishable from Reinke crystals. The Leydig-like cell-nonmyelinated nerve complexes, noted in both the adrenal cortex and medulla, showed perivascular localization, and their morphologic features were similar to those of hilus cells of the ovaries or extraglandular Leydig cells of the testis. The underlying mechanism accounting for the development of Leydig-like cells remained obscure; cytodifferentiation from pluripotent mesenchymal cells, possibly mediated by secretory products of sympathetic nerve fibers, may provide an explanation for their formation.
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PMID:Leydig-like cells in the adrenals of a woman with ectopic ACTH syndrome. 719 May 43

We evaluated three cases of pigmented pulmonary carcinoid tumors that were retrieved from the files of the Armed Forces Institute of Pathology, Washington, DC. Clinical follow-up showed no indication of tumor recurrence or metastases, nor was there evidence of malignant melanoma. All three cases exhibited histologic features of typical carcinoid tumor; there were focal oncocytic changes in two cases. Finely dispersed, brown pigment, believed to be melanin, was distributed in two different patterns: in sustentacular cells (case 1) or within the tumor cells (cases 2 and 3). Fontana-Masson stain was positive in areas of this pigment in all cases. The tumor cells showed immunoreactivity for chromogranin, synaptophysin, keratin (AE1/AE3 and CAM-5.2), and S100 protein in all cases. Focal staining for vimentin and corticotropin was seen within neoplastic cells in two cases. The pigmented sustentacular cells in case 1 showed focal immunoreactivity for S100 protein and HMB-45. Ultrastructural studies of paraffin-embedded tissues were performed in two cases. They showed well-developed melanosomes in the pigmented sustentacular cells in case 1. In both cases, cytoplasmic neurosecretory-type granules were identified in neoplastic cells. These findings demonstrate that pigmented pulmonary carcinoid tumor has an immunohistochemical profile similar to that of typical pulmonary carcinoid tumor. In some instances, pigmented pulmonary carcinoid tumors may show ultrastructural evidence of melanocytic and neuroendocrine differentiation. These immunohistologic and ultrastructural findings distinguish pigmented pulmonary carcinoid tumor from malignant melanoma and support the concept of "multidirectional cellular differentiation."
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PMID:Pigmented pulmonary carcinoid tumor. An immunohistochemical and ultrastructural study. 768 14

Various factors that modulate the differentiation of malignant cells are known to affect their experimental metastatic potential (EMP), or lung colonization after intravenous injection into syngeneic animals. However, some results and conclusions on the relation between cell differentiation and metastasis have appeared to conflict. We have reanalysed this by measurement of EMP of B16 melanoma sublines after culture with agents or conditions that acted on differentiation through various intracellular pathways. All tested agents did affect the EMP. EMP was usually positively correlated with differentiation under diverse conditions, but exceptions showed that there is no direct causal connection. Nor could all findings be explained in terms of cell proliferation or expression of major histocompatibility antigens. Some data helped to explain disparities between previous reports. Specific novel findings included the following. The stimulation of EMP by melanocyte-stimulating hormone (MSH) as well as all other tested effects of MSH were prevented by extended exposure to 12-O-tetradecanoyl phorbol acetate (TPA), suggesting a requirement for protein kinase C activity as well as G-protein coupling in MSH action. Cells grown with cholera toxin were always more differentiated than untreated cells, but the EMP could be either markedly increased or markedly decreased by cholera toxin under different conditions. The basic culture medium apparently determined this striking reversal. The EMP was also significantly affected by the extracellular pH.
Clin Exp Metastasis 1994 Nov
PMID:Experimental metastasis and differentiation of murine melanoma cells: actions and interactions of factors affecting different intracellular signalling pathways. 792 91


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