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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of diabetes mellitus on the course of breast cancer was investigated retrospectively in 752 patients. Possible unfavourable prognostic factors like overweight, lipid disorders, age and menopausal status were considered as confounders in a Cochran-Mantel-Haensel analysis. There was no difference in primary tumor status and lymph node involvement between patients with diabetes mellitus and nondiabetic patients. Diabetic patients had more often overweight, lipid disorders and were older than nondiabetic patients. Metastatic disease was highly significant correlated with primary tumor status (p less than 10(-6)) lymph node involvement (p less than 10(-10)) and diabetes mellitus (p less than 10(-5)). Overweight, lipid disorders, age and menopausal status were not correlated with metastatic disease. A possible explanation of the correlation between diabetes mellitus and metastatic disease could be hyperinsulinism in type IIB diabetes. A type IIB diabetes in most of the patients included in this study is very plausible because of the correlation between overweight, lipid disorders, old age and diabetes mellitus. This type of diabetes is characterised by a relative resistence to insulin in the target tissues and a prolonged and exceeding insulin secretion. Experimental data demonstrate that insulin stimulates the growth of breast cancer cell in vivo and in vitro.
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PMID:[Diabetes mellitus and breast cancer. A retrospective follow-up study]. 218 18

In the present study of 45 patients with Zollinger-Ellison syndrome, the frequency and clinical importance of the release of multiple gastrointestinal peptides were assessed prospectively. During an initial evaluation, extent of gastrinoma, clinical symptoms, disease duration, and presence or absence of multiple endocrine neoplasia, type I (MEN-I) were assessed. All patients had determinations of fasting plasma gastrin, human pancreatic polypeptide, motilin, neurotensin, and somatostatin; 35 had determinations of insulin and gastrin-releasing peptide and 21 had determinations of glucagon. A plasma elevation of additional peptides besides gastrin was detected in 62%, with 44% having one, 18% having two, and 0% having three additional peptides elevated. Motilin was elevated in 29%, human pancreatic polypeptide in 27%, neurotensin in 20%, and gastrin-releasing peptide in 10%, whereas insulin, glucagon, and somatostatin were not elevated in any patient. The presence or absence of elevation of any peptide did not differ in patients with or without MEN-I, with gastrinoma size, with the presence or absence of metastatic disease, or with various clinical symptoms. Patients were assessed yearly for clinical evidence of a secondary symptomatic pancreatic endocrine tumor syndrome with a median follow-up of 146 and 84 months from onset or diagnosis, respectively. Only one patient (2% of patients) developed a second syndrome (rate, 2 patients per 100 patients observed for 10 years). These results demonstrate that the plasma elevation of multiple gastrointestinal peptides is common in patients with Zollinger-Ellison syndrome; however, the rate of developing a second symptomatic pancreatic endocrine tumor syndrome is much lower than generally believed. Furthermore, no evidence is found to support the conclusions that the detection of the plasma elevation of these peptides is clinically important in assessing MEN-I status, disease extent, or presence of metastatic disease or that elevated levels of motilin, neurotensin, gastrin-releasing peptide, or human pancreatic peptide are associated with any distinct clinical symptoms. Therefore, we recommend that plasma concentrations of these additional gastrointestinal peptides should not be assessed routinely but rather only if new symptoms develop.
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PMID:Multiple hormone elevations in Zollinger-Ellison syndrome. Prospective study of clinical significance and of the development of a second symptomatic pancreatic endocrine tumor syndrome. 222 72

Based on observations of five of own patients the author analyzes the causes of spontaneous hypoglycaemia in malignant tumours and assumes three mechanisms of development: 1. Metastatic affection of the liver reduces the reserves of homeostatically usable glycogen and can reduce also the amount of utilized insulin and glucagon, and this weakens the effectivity of contraregulating hormones. 2. In case of large mesenchymal tumours it is assumed that the cause of hypoglycaemia is the neoplastic formation of IGF II. For these hypoglycaemic states a low concentration of C-peptide, IRI (immunoreactive insulin), absence of response of growth hormone to hypoglycaemia, high IGF II in the tumour and plasma and high mRNA for IGF II in the tumour is typical. 3. In hypoglycaemic states with massive metastases in the liver, high IRI and C-peptide it is assumed the cause of hypoglycaemia is a metastatizing insular tumour or a nes.dioblastoma. In those instances concurrent peptic ulcers (gastrin production) are frequent.
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PMID:[Neuroglycopenic syndromes in malignant tumors]. 225 61

Eighty-four carcinoids of the colon and rectum were studied with emphasis on prognostic features, immunohistochemical characteristics, and pitfalls in diagnosis. Follow-up data were available on 35 patients. Tumors with adenocarcinomatous components, or those resembling small cell carcinomas of the lung, were excluded. Eighty-one tumors were in the rectum and three tumors were in the distal sigmoid colon. Neuron-specific enolase, chromogranin, and Leu-7 were positive in 87%, 58%, and 53% of the tumors, respectively. Hormones were positive in the following percentages: serotonin, 45%; pancreatic polypeptide, 46%; glucagon, 10%; gastrin, 3%; somatostatin, 3%; adrenocorticotrophic hormone, 1%; cholecystokinin, 0%; calcitonin, 0%; and insulin, 0%. Many tumors elaborated more than one hormone. Fifty-five percent of the tumors were argyrophil and 28% were argentaffin. Carcinoembryonic antigen was present in 24% of the tumors; 82% of the tumors contained prostatic acid phosphatase. Three patients had liver metastases; their tumors ulcerated, invaded muscularis propria, and had more than 2 mitoses per 10 high-power fields (HPF). One patient with a 2.5-cm tumor without mitoses had regional lymph node metastases. All non-metastasizing tumors had less than one mitosis in 10 HPF. We conclude that large bowel carcinoid tumors are essentially limited to the rectum and sigmoid, that they are indolent if mitotically inactive and smaller than 2 cm, and that most show production of a selected group of endocrine markers.
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PMID:Rectal and colonic carcinoids. A clinicopathologic study of 84 cases. 229 59

The nuclear DNA content of 17 pancreatic neuroendocrine tumors was measured from paraffin-embedded tissue with flow cytometry. The tumors were classified by immunostaining with antisera for synaptophysin, insulin, gastrin, glucagon, pancreatic polypeptide, somatostatin, and vasoactive intestinal polypeptide. Eight (47%) of the 17 tumors were aneuploid, and two (12%) were multiploid (had two aneuploid stemlines of cells). Seven of the eight insulinomas, one of the four gastrinomas, and two of the four nonspecified neuroendocrine tumors had an abnormal nuclear DNA content. The DNA indices of the aneuploid and multiploid cases ranged from 1.13 to 1.93, and three cases had a DNA index greater than 1.50. During the follow-up for up to 16 years (mean, 7 years), one patient with diploid nonspecified tumor died of the disease, another patient with a multiploid gastrinoma had metastatic disease develop, and a third patient with a multiploid nonspecified tumor was alive with the disease. The authors conclude that many neuroendocrine tumors of the pancreas have an abnormal nuclear DNA content as measured by DNA flow cytometry. DNA multiploid pancreatic neuroendocrine tumors may be associated with a less favorable clinical course, but this needs to be confirmed in additional studies.
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PMID:DNA ploidy in pancreatic neuroendocrine tumors. 234 35

Digestion of primary breast cancers and their metastases with collagenase yields cell clusters which can be selectively isolated from stromal cells and from the less malignant-looking epithelium of the primary tumors by their failure to attach as rapidly to collagen gel. Continued passage in culture of one preparation of cell clusters has yielded a continuously growing cell strain, termed Ca2-83. This strain continues to grow mainly as cell clusters with doubling times of 10 to 14 days, although some clusters eventually adhere to plastic substrata. Two morphological extremes of cell were observed, smaller polygonal or cuboidal cells and larger, often-multinucleated cells which contain fat droplets. Cell clusters grew in a gland-like pattern similar to those of the original carcinoma and formed small nodules in 50% of recipient nu/nu mice. Both morphological forms of Ca2-83 in culture or in tumor nodules stained immunocytochemically with epithelial cell-specific antisera to epithelial membrane antigens and to human keratins but not to laminin or actin. Cultures of Ca2-83 failed to synthesize laminin under conditions where its synthesis was observed in a rat myoepithelial cell line. Ultrastructural analysis of the cell clusters has identified microvilli coated with epithelial membrane antigens and junctional complexes typical of secretory epithelia in both morphological forms, but no characteristics of myoepithelial cells or basement membranes were observed. The DNA content of the cultures increased in response to serum, a bovine pituitary fraction, and insulin. Numbers of cell clusters were also increased in the presence of culture medium exposed to preadipocytes, myoepithelial- or mesothelial-like cells/stromal cells, or to prostaglandin E2.
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PMID:Loss of production of myoepithelial cells and basement membrane proteins but retention of response to certain growth factors and hormones by a new malignant human breast cancer cell strain. 241 Jan 3

The increased knowledge of the pathobiology of gastrointestinal and pancreatic neuroendocrine tumours and the improved therapeutic possibilities have brought a demand for more precise diagnosis. Although the neuroendocrine tumours can often be tentatively recognized in routinely processed microscopic slides, their more accurate identification requires additional diagnostic procedures. General neuroendocrine markers, such as the argyrophil reaction of Grimelius and immunohistochemistry with application of antibodies against chromogranin A and of neuron-specific enolase are discriminatory staining methods which are used to reveal the neuroendocrine origin of almost all highly differentiated neuroendocrine tumours of the gastrointestinal tract (carcinoids) and pancreas (insulomas). Midgut carcinoids, which predominate among these tumours almost unexceptionally contain serotonin. This biogenic amine can be demonstrated by the argentaffin reaction of Masson, serotonin immunoreactivity or by formalin-induced fluorescence. The characteristic staining pattern of midgut carcinoids is almost invariably preserved in the metastases and can thus be used to reveal a primary midgut carcinoid. The enterochromaffin-like (ECL) cell carcinoids of the body and fundic area of the stomach are argyrophil with Sevier-Munger silver stain. Other neuroendocrine tumours, viz, antral, duodenal and rectal carcinoids and insulomas, should be studied by a battery of relevant peptide hormone antisera for adequate diagnosis. About 50% of all insulin-producing insulomas are endowed with stromal amyloid deposits, which chemically are composed of a peptide designated islet amyloid polypeptide. This molecule has been observed by electron microscopical immunocytochemistry to occur exclusively in the beta-cells and is co-stored with insulin in the beta-cell granules.
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PMID:Diagnostic pathology of gastrointestinal and pancreatic neuroendocrine tumours. 247 24

Eighteen cases of insulinoma treated at the Instituto Nacional de la Nutricion in Mexico City are presented. The cases were operated on between 1959 and 1988, and include 10 women and 8 men with a mean age of 38. The duration of symptoms ranged between 4 and 96 months with a median of 27; 78% of the patients had neuropsychiatric symptoms, 61% seizures, and 55% loss of consciousness. One of the patients had evidence of type I multiple endocrine neoplasia. Diagnosis was established in all the patients with the demonstration of Whipple's triad and also with an elevated insulin determination in the last nine patients. In six cases the insulinoma was enucleated; in two a Whipple procedure was performed; in nine a distal pancreatectomy and in the remaining patient only resection of hepatic metastases; 67% of the tumors were diagnosed as benign solitary adenomas, 16.5% as carcinomas and the same number as hyperplasia. Operative mortality was 5.5%, and morbidity 44%. The three carcinomas survived 6, 8 and 36 months. Disappearance of the hypoglycemic symptoms was obtained in 93% of the cases of adenoma and hyperplasia.
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PMID:[Surgical treatment of insulinoma. Experience at the Salvador Zubiran National Nutrition Institute]. 255 Oct 25

Proliferation of endocrine cells was found to occur during early, i.e., first 12 weeks, exocrine pancreatic carcinogenesis after 6 weekly treatments of Syrian hamsters with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). Cells containing insulin (Ins), glucagon (Glu), and somatostatin (Som) were noted in all stages of tumor development and were present in adenocarcinomas and in metastases to the liver. Some of the cancer cells were of amphicrine (hybrid) type, i.e., produced both mucin and endocrine substances. Measurement of these hormones revealed a significant decrease in plasma Ins during early stages of carcinogenesis with concomitant increase of Ins level in pancreatic juice at 12 weeks after 6 weekly BOP treatments. Plasma Glu and Som were not changed. The changes noted, particularly in relation to Ins, suggest that proliferation of endocrine cells in pancreatic carcinogenesis may be associated with alterations in hormone secretion.
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PMID:Alteration of pancreatic endocrine cell patterns and their secretion during pancreatic carcinogenesis in the hamster model. 257 21

Twenty-one cases of cutaneous neuroendocrine (Merkel cell) carcinoma (CNEC) were examined by the ABC-immunoperoxidase method with a panel of antibodies to 5 intermediate filaments, 6 neuroendocrine-associated antigens, 6 peptide hormones, as well as melanoma-associated cytoplasmic antigen (HMB-45) and leukocyte common antigen. All tumors showed strong cytokeratin staining in characteristic dense, inclusion-like, cytoplasmic globules and in a reticular peripheral cytoplasmic pattern. Cytoplasmic coexpression of inclusions of neurofilament antigen was observed in 9/21 cases. Staining for one or more neuroendocrine markers in formalin-fixed tissue (bombesin, 7/20; chromogranin, 11/21; synaptophysin, 6/21) was weak and focal but present in 17/21 cases. In 3 cases, sections of unfixed, snap-frozen tumor were compared with formalin-fixed tissue, and these showed strong, diffuse staining for multiple neuroendocrine antigens. Immunostaining for peptide hormones was not observed, with the exception of weak, focal staining for insulin (1 case), calcitonin (1 case) and somatostatin (2 cases). In 13 cases DNA indices and S-phase fractions (SPF) were determined by flow cytometry on nuclear suspensions from paraffin blocks. DNA histograms in 12 of 13 cases had normal range DNA content (diploid) and elevated S-phase fractions (mean 15%, range 8 to 22%). Mean SPF was not significantly different in the group of patients who developed recurrent and/or metastatic disease (15.6%, N = 10) compared with patients without recurrence (15.8%, N = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cutaneous neuroendocrine (Merkel cell) carcinoma: an immunophenotypic, clinicopathologic, and flow cytometric study. 266 40


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