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)

A recurred and metastasized hemangiopericytoma of menigeal origin caused a terminal hypoglycemia syndrome in a 40 year old man. The disease had been observed over a period of 10 years. The total weight of the tumour metastases was 1800 g. Electron microscopical examination of the tumour cells revealed, in particular, a markedly developed ergastoplasm, prominent Golgi complexes surrounded by many microvesicles, round to ovoid electron dense bodies and fine fibrillar structures. Furthermore, large deposits of basement membrane-resembling material were found in the pericapillary and intercellular spaces. On the basis of the structural characteristics which indicate distinct synthesizing capacity of the cells, an excessive glucose consumption by the tumour is suggested to be an important factor in the pathogenesis of tumour hypoglycemia. The question whether the ultrastructure of the tumour also exhibits secretory processes, which may be related to the release of a presumed inhibitor of hepatic gluconeogenesis and/or glycogenolysis, remains open. Typical granules as in polypeptide hormon secreting cells were not observed. The possibility that the demonstrated electron dense membrane limited bodies represent atypical secretory granules is discussed.
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PMID:Ultrastructure of hemangiopericytoma associated with paraneoplastic hypoglycemia. 13 25

A 40-year-old man with the Verner-Morrison syndrome (refractory watery diarrhoea and hypokalaemia in islet-cell tumour of the pancreas) had an islet-cell carcinoma of the non-B-cell type with metastases to liver and mesenteric lymph nodes. High concentrations of a vasoactive intestinal polypeptide (VIP) were demonstrated in tumour tissue and plasma by radioimmunological tests. After surgical removal of the tumour the plasma VIP concentration fell to normal. Immunohistochemical tests of the tumour for gastrointestinal hormones demonstrated marked fluorescence only for vaso-active intestinal polypeptide. It is assumed that this polypeptide is largely responsible for the clinical signs. In the described case the severe watery diarrhoea ceased after glucocorticoid administration.
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PMID:[The vaso-active intestinal polypeptide in Verner-Morrison syndrome]. 16 27

A 61-year-old woman had watery diarrhea, hypochlorhydria, hypokalemia, and elevated serum gastrin levels. She had islet cell carcinoma of the body of the pancreas with multiple metastases to the liver. Radioimmunoassay and immunofluorescence demonstrated both vasoactive intestinal polypeptide (VIP) and gastrin in the surgically removed carcinoma and in a metastatic focus. Electron microscopical findings confirmed the presence of two cell types whose secretory granules had characteristics ascribed to these two hormones. Plasma prostaglandin E levels were also elevated above normal. Serum VIP levels became elevated to the Verner-Morrison range prior to her death of a bleeding duodenal ulcer two years after initial symptoms.
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PMID:Vasoactive intestinal polypeptide and gastrin-producing islet cell carcinoma. 19 71

A patient is described who presented with the classical symptomatology and profound electrolyte disturbance of the Verner-Morrison syndrome due to a pancreatic apudoma secreting vasoactive intestinal polypeptide (VIP). Diagnosis was confirmed by plasma VIP as measured by a radio-immunoassay technique now available. It is suggested that the cyclical nature of the symptoms in this case was due to cyclical release of VIP from the tumour in response to an unknown stimulus. Perfusion studies confirmed the excess secretory state of water, sodium and chloride in the small intestine. Symptoms were completely abolished by surgery and the progress is being monitored by means of serial plasma VIP estimations to detect any early recurrence of metastatic disease.
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PMID:Cyclical release of vasoactive intestinal polypeptide (VIP) from a pancreatic islet cell apudoma. 21 90

Carcinoma of the bronchus can produce several polypeptide hormones and therefore has the capacity to cause most syndromes of endocrine hyperfunction. All pituitary hormones can be synthesized ectopically; furthermore, the production of hormones from the hypothalamus (CRF), the placenta (HCG, HPL) and the C-cells of the thyroid (calcitonin), as well as parathormone and prostaglandins has been described. The paraneoplastic syndrome may often be more dangerous for the patient than the tumor growth itself, and can lead to early death. On the other hand, it may allow the early detection of an unsuspected tumor. The ectopic hormones and other nonendocrine proteins and peptides can be used as tumor markers, and can demonstrate the effect of treatment and early recurrence or metastases. An ideal tumor marker should have the following characteristics: 1. production exclusively by neoplastic tissue, 2. direct correlation with tumor size, 3. substances common to all tumor types ("large spectrum tumor marker") although specific tumor markers for special tumors should be available, 4. the assays must be easy and automation should be possible. At present no tumor marker satisfies all these conditions. The measurement of several tumor markers and the use of discriminant analysis may extend their diagnostic value and open the way for biochemical detection of cancer in the future.
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PMID:[Ectopic hormone formation and tumor markers in bronchial neoplasms]. 22 36

We evaluated assays of Tissue Polypeptide Antigen in serum and urine, as an index to the presence of cancer. In the assay, serum, which is first absorbed with human albumin-labeled sheep erythrocytes, or untreated urine (diluted with an equal volume of TPA-free serum) is incubated with antibody specific to Tissue Polypeptide Antigen and then reacted with sheep erythrocytes labeled with Tissue Polypeptide Antigen. We found an increased concentration of Tissue Polypeptide Antigen in the serum of 378 of 513 (74%) and in the urine of 49 of 77 (64%) patients with cancer, as compared with 40/112 (36%) and 7/29 (24%), respectively, for individuals with benign neoplasms. Normal individuals were defined as those with less than 0.09 unit of the antigen per milliliter of specimen. Concentrations exceeding this were found in 2/67 (3%) sera and 6/56 (11%) urines from supposedly normal persons. Tissue Polypeptide Antigen was found in above-normal concentrations in patients with cancer, regardless of neoplasm type and extension, with a higher proportion of abnormal values in patients with distal metastases.
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PMID:A preliminary evaluation of tissue polypeptide antigen in serum or urine (or both) of patients with cancer or benign neoplasms. 65 73

This report documents a case of a fatal primary malignant neoplasm of the liver with metastases to the lymph nodes of the porta hepatis and the pubic bone. Profound, intractable hypoglycemia was seen during the course of the disease. No immunoassayable insulin was found in the blood during episodes of severe, symptomatic hypoglycemia. The neoplasm was composed of uniform polygonal cells with distinct cytoplasmic borders growing in broad strands with a tendency toward nesting and was morphologically similar to neoplasms of neural crest derivation. The presence of osmophilic, membrane-bound granules in the neoplastic cells was documented by ultrastructural studies. The tentative conclusion that the hypoglycemia was produced by the secretion of a substance with insulin-like activity, probably a polypeptide, by the secretory granules in the neoplastic cells is supported by clinical and laboratory data.
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PMID:Malignant apudoma of the liver with symptomatic intractable hypoglycemia. 67 61

The recent findings regarding the possible relation of prolactin to human breast cancer are reviewed. Prolactin is a single-chain polypeptide hormone secreted by the anterior pituitary; it appears important to the development and growth of mammary tumors in mice and rats. Certain drugs (L-dopa, the ergot derivatives) inhibit the release of prolactin from the anterior pituitary and lower its serum concentration. Chlorpromazine and other phenothiazines block the synthesis, release, or action of prolactin-inhibiting factors leading to increased prolactin secretion. The midcycle serum estrogen elevation does not increase serum prolactin but often high doses of estrogen will. Mammary tumors in mice and rats appear different from those in human, being of alveolar origin while human tumors are thought to be ductal. Also, rodent cancers do not usually metastasize, even when large. About 40% of human breast cancers respond to endocrine therapy while in Sprague-Dawley rats induced mammary tumors are 80% hormone responsive. In mice hyperplastic nodules but not mammary cancers respond to horomone deprivation. Prolactin is a key hormone in the stimulation of hyperplastic nodules in mice and mammary tumors in rats. The effects of progesterone on these growths is not clear. Serum prolactin levels normally vary throughout the day. Levels are not different in cancer patients but certain families with high cancer rates have been shown to have higher than normal serum levels. Although prolactin receptors have been identified in mouse and rat mammary tissue and tumors and prolactin responsiveness of the tumors correlated with the number of such receptors, these receptors have not been identified in human breast cancer cells. Patients have responded to L-dopa with relief of bone pain and a 50% decrease in serum prolactin. Suppressing atypical precancerous lesions by depriving them of their hormonal support offers the best chance for preventing eventual development of breast cancer. In vitro determination of the presence of prolactin receptors in human breast tumor tissue may allow accurate prediction of response to endocrine ablation. Variations in prolactin receptors may account for response differences of breast tumors to different doses of estrogen. Near-zero prolactin levels following hypophysectomy in some patients have been correlated with clinical remissions. Combinations of drugs to reduce serum prolactin levels or antagonize the hormones's effect on the breast may be needed to obtain results.
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PMID:Prolactin and breast carcinoma. 108 86

The presence in tumors of numerous cytokines suggests that they potentially modulate tumor cell activities and host tissue remodelling. To investigate the possible involvement of transforming growth factor type beta (TGF beta) in the metastatic process of cancer development, we have studied the effect of this factor on two rat colon carcinoma cell lines. These cell clones had been previously tested and selected for their ability to develop metastases in syngenic animals or lack of it. The two cell lines were characterized for their production of TGF beta. Production of active and latent forms of TGF beta 1 in the medium conditioned by the rat colon cancer cells were quantified using a bioassay. The presence of active TGF beta 1 was demonstrated in conditioned medium from the progressive tumor (PROb) cells and significant expression of latent forms of TGF beta 1 were found in the conditioned media from both cell clones. TGF beta 1 slightly inhibited proliferation of PROb cells which had been previously described as moderately differentiated, and significantly stimulated proliferation of the regressive (REGb) cells, described as poorly differentiated. On the basis of our observations, we suggest that this endogenous factor could be involved in autocrine regulation of tumor cell activities and in paracrine regulation of stroma cell and immune responses. Active and/or latent expression of TGF beta 1 by the two rat colon carcinoma cell lines, and their variable responses to the growth factor, strongly suggest that this polypeptide is involved in the regulation of tumorigenic expression of adenocarcinoma cells.
Invasion Metastasis 1992
PMID:Possible involvement of TGF beta 1 in the distinct tumorigenic properties of two rat colon carcinoma clones. 133 1

Fifty exocrine pancreatic adenocarcinomas and 57 benign tumors induced in Syrian hamsters by N-nitrosobis(2-oxopropyl)amine (BOP) were examined for the presence of argyrophil cells antiinsulin, -glucagon, -somatostatin, -pancreatic polypeptide (PP), -gastrin/CCK, -vasoactive intestinal polypeptide (VIP), and - neuron-specific enolase (NSE) reactive cells. Argyrophil - and antihormone-reactive cells were found in the normal pancreatic ducts and in the acini, as well as in hyperplastic and atypical ducts/ductules, tubular complexes, benign lesions, and in 80% of ductal adenocarcinomas. Insulin and antiNSE-reactive cells were the most common, followed in decreasing frequency by glucagon, somatostatin, and PP cells. Antigastrin-/CCK-and -VIP-reactive cells were found in two cases. Argyrophil cells were present in about 60% of the tumors with Grimelius staining and in 55% of those with Churukian-Schenk staining. Insulin cells were seen in ductal cancer that had grown into a lymph node and in the lymph node metastases of another cancer. A novel finding was the presence of argyrophil and insulin cells within the lumen of some malignant glandular structures. Coexistence of several peptide cells was found in 52% of the cancers. The presence of argyrophil and hormone-producing cells in induced pancreatic ductal/ductular lesions further strengthens the existence of a close developmental relationship between exocrine and endocrine cells of the pancreas.
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PMID:Immunohistochemical characterization of endocrine cells in experimental exocrine pancreatic cancer in the Syrian golden hamster. 135 11


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