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 molecular forms of ACTH secreted by established human small cell lung cancer (SCLC) cells and primary cultures derived from a bronchial carcinoid tumour, a pituitary adenoma and hyperplastic pituitary tissue have been characterized by Sephadex G-75 chromatography and quantified with two novel immunoradiometric assays for ACTH and ACTH precursor peptides. Pro-opiomelanocortin (POMC; Mr 31,000) and pro-ACTH (Mr 22,000) were secreted by all cell types. No smaller peptides were identified in the culture media from SCLC and bronchial carcinoid cells, implying a deficiency in the enzymes and/or intracellular organelles required for extensive POMC processing. A more heterogeneous profile of ACTH-containing peptides was produced by cells of pituitary origin, indicating more extensive proteolytic processing of POMC. However, the major peptide secreted by cells from a large aggressive pituitary adenoma was unprocessed POMC (Mr 31,000). These results suggest that both lung and pituitary cells in vitro retain their in-vivo pattern of POMC processing and provide valuable models in which to study the regulation of ACTH synthesis and secretion.
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PMID:Comparison of ACTH and ACTH precursor peptides secreted by human pituitary and lung tumour cells in vitro. 215 69

Ten patients with hepatic metastases from islet cell tumors or carcinoid tumors had clinical symptoms from hormonal secretion and/or pain related to the mass effect of neoplastic liver involvement. Hepatic arterial embolization (HAE) using radiographically guided catheters to inject thrombogenic material was applied to the right and/or left hepatic arteries separately 5 to 7 days apart. All ten patients improved within days of the procedure as confirmed by a decrease in measurable hormone levels (gastrin, adrenocorticotropin, and 5-hydroxy indole acetic acid) or by a decrease in tumor size and improved symptoms. Three patients underwent repeated reembolization from two to four times over nine to 50-month intervals for symptom control. Complications of and indications for HAE in these patients are discussed. It appears to be an effective treatment for dealing with the hormonal syndromes and local symptoms related to the hepatic metastases of hormone-secreting tumors.
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PMID:Hepatic arterial embolization for metastatic hormone-secreting tumors. Technique, effectiveness, and complications. 216 Dec 78

The association of a bronchial or thymic carcinoid as a source for the ectopic production of adrenocorticotropic hormone (ACTH) has been reported since 1957, with approximately 72 cases in the literature. These patients are characterized by young age, long duration of Cushing's syndrome because of the inability to find the ectopic source, and a high incidence of hypophysectomy or adrenalectomy without curing the disease. A substantial number of patients, upon discovery of the thoracic ectopic source, are also found to have malignant carcinoid tumors with lymph node metastases. Fifteen patients have been explored for a presumed intrathoracic source of ACTH at our institution since 1983 and 14 carcinoids (13 bronchial, one thymic) have been resected. Seventy-one percent (10/14) of the patients appear cured with normal plasma ACTH levels 5 to 57 months after resection, despite a 50% incidence of positive lymph node disease. Management of these patients demands an aggressive evaluation to prevent unnecessary adrenalectomy or hypophysectomy and to allow earlier resections before these potentially curable malignancies metastasize. When the tumor is discovered, thorough exploration and complete lymph node mapping with resection must be performed.
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PMID:Management of the ectopic ACTH syndrome due to thoracic carcinoids. 216 61

A 36-year-old patient developed marked pigmentation, marked myopathy and severe hypokalaemic alkalosis which at first pointed towards an ectopic ACTH syndrome. The dexamethasone test at a high dose indicated cortisol suppression. A mediastinal tumour was seen radiologically, but the sella was of normal size. Computed tomography provided indirect signs of a sellar space-occupying lesion which suggested an ectopic production of corticotropin-releasing factor (CRF) as cause of the Cushing's syndrome. CRF concentration in antecubital venous blood was markedly elevated to 280 ng/l. The mediastinal tumour was excised and proved to be a carcinoid histologically. Postoperatively the CRF concentration fell to 70 ng/l. An extract of the carcinoid contained 15.5 ng/g wet-weight of CRF and 254 ng/g wet-weight of beta-endorphin. The patient died 5 weeks postoperatively of sepsis with bilateral pneumonia. At autopsy the hypophysis was of normal size but showed nodular ACTH-cell hyperplasia. This was thus a case of Cushing's syndrome resulting from ectopic CRF production in a mediastinal carcinoid tumour.
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PMID:[Cushing's syndrome in CRF-producing mediastinal carcinoid]. 230 1

It is well known that carcinoid tumors and some small-cell carcinomas of the lung contain dense-core granules (DCGs). Moreover, a small number of tumors presenting with epidermoid, large-cell, or adenocarcinoma histologic characteristics (so-called atypical endocrine tumors), also contain DCGs. Herein, we describe certain histochemical features of DCG tumors and compare them with other major lung tumor types that lack DCGs (non-DCG tumors). All DCG tumors contained neuron-specific enolase and many contained serotonin. These markers were not present in any non-DCG tumor. Other histochemical markers (glycogen, mucosubstances, corticotropin, beta-human chorionic gonadotropin, keratin, somatostatin, and calcitonin) were found in a proportion of DCG and non-DCG tumors, but were, in general, more common in non-DCG tumors and atypical endocrine tumors than in carcinoids and small-cell carcinomas. alpha-Fetoprotein was rarely found in non-DCG tumors, and was never observed in DCG tumors. The atypical endocrine group represents a class of tumors with a remarkably mixed and varied phenotype. Their potential significance is discussed and methods to facilitate their diagnosis are suggested.
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PMID:Histochemical studies of dense-core granulated tumors of the lung. Neuron-specific enolase as a marker for granulated cells. 240 47

In order to establish the extent of neuroendocrine differentiation and the occurrence of neurohormonal peptides in the neoplastic cells of prostatic carcinomas, silver-staining and immunocytochemical techniques were used. All gave satisfactory results. The incidence of the neuroendocrine cells seemed to be higher in the fresh "Bouin-fixed" biopsy specimens than in the conventionally "formalin-fixed" specimens from archival paraffin blocks. All carcinomas demonstrated argyrophil cells as an integral element of the tumour. In highly differentiated carcinomas (grade I) these cells were scattered focally, intermingled with non-argyrophil cells in typical adenocarcinomas; their incidence was estimated to be about the same as in benign prostatic hyperplasia. Most of them were immunoreactive with antisera raised against serotonin and/or TSH (thyroid stimulating hormone). In moderately and poorly differentiated (grades II-III) carcinomas, however, the argyrophil cells were more numerous and showed greater variation in growth pattern; only occasionally they displayed a typical carcinoid-like structure. Moderately and poorly differentiated carcinomas also showed a greater variation in the number and kinds of peptide immunoreactivities than the highly differentiated carcinomas. In addition to serotonin- and TSH-immunoreactive cells as the most prevalent type, now also human chorionic gonadotrophin (HCG-alpha), adrenocorticotropic hormone (ACTH), leu-enkephalin, beta-endorphin, somatostatin, glucagon and calcitonin immunoreactive cells could be found within certain tumour areas and often with a distinctly patchy distribution. In two cases, where the tumour cells in the metastases were also investigated, they were found to be both argyrophil and immunoreactive with the same antisera as those of the primary tumour. Our findings emphasise the fact that prostatic carcinomas are more complex and heterogenous than previously thought, exhibiting endocrine differentiation as an integral element of virtually all prostatic adenocarcinomas.
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PMID:Peptide-hormone- and serotonin-immunoreactive tumour cells in carcinoma of the prostate. 244 32

Neuroendocrine differentiation in prostatic neoplasms has in the past been considered extremely uncommon. The histologic neuroendocrine patterns reported previously vary from small cell to carcinoidlike to mixed adenocarcinoma--small cell or carcinoid. The majority of the tumors reported are of the mixed variety. We reviewed 2648 autopsies, revealing 69 prostatic carcinomas, eight with neuroendocrine differentiation (five mixed adenocarcinoma--small-cell carcinoma, two "pure" small cell, and one "pure" carcinoidlike). The mean patient age was 69.5 years. One patient presented with markedly elevated serum corticotropin and another was severely hypercalcemic with elevated serum parathyroid hormone level. Three neoplasms were incidental autopsy findings. The mean survival time, after diagnosis, was 19 months for the other patients. Three of the cases were examined ultrastructurally and showed cytoplasmic processes containing membrane-bound granules in the neuroendocrine component. The areas with neuroendocrine differentiation were positive for markers as follows: neuron-specific enolase, seven of eight; prostate-specific antigen (PSA), none of eight; chromogranin A, seven of eight; synaptophysin, four of eight; and calcitonin, four of eight. Those neoplasms mixed with an adenocarcinoma component showed well-defined PSA positivity in the glandular elements. This study suggests that neuroendocrine differentiation in prostatic neoplasms may be more common than previously thought. Often, the areas with neuroendocrine differentiation are considered to represent poorly differentiated adenocarcinoma. It is important to recognize neuroendocrine components in prostatic carcinomas owing to prognostic and potential therapeutic implications.
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PMID:Neuroendocrine differentiation in prostatic carcinomas. A retrospective autopsy study. 246 64

Because so-called 'carcinoid' tumour of the breast has proven to be a difficult entity to define, we studied in-situ carcinoma as there were reasons to believe that this might help clarify the complex problems involved. We studied a consecutive series of 30 cases of ductal carcinoma in-situ (DCIS) by light microscopy and silver impregnation methods and identified a relatively common endocrine variant of DCIS. This variant was studied by immunocytochemical and ultrastructural methods, using conventional DCIS as a control. Endocrine DCIS is identified by its organoid pattern, stromal 'inclusions', festooned structure and a distinctive type of polypoid invagination. It is argyrophilic and rich in neuron-specific enolase. Ultrastructurally it contains abundant dense core granules which are impregnated selectively by Grimelius' method. This tumour type frequently contains peptide hormones of the ACTH family. Three of seven cases contained cells reactive for ACTH and corticotropin-like intermediate lobe peptide CLIP or their precursor, pro-opiomelanocortin. A fourth tumour contained neurotensin, recently identified in a variety of endocrine tumours. Argyrophil invasive carcinomas are a much more heterogeneous group of tumours than argyrophil DCIS and only a minority have an endocrine structure comparable to that described here.
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PMID:A morphological and immunocytochemical study of a distinctive variant of ductal carcinoma in-situ of the breast. 1789 2

Cushing's syndrome due to bronchial carcinoid tumors that secrete adrenocorticotropin (ACTH) may be difficult to distinguish from pituitary Cushing's disease, since the responses to dexamethasone and metyrapone are sometimes similar. Recently, the ACTH and cortisol responses to ovine corticotropin-releasing factor (oCRF) have been shown to be different in pituitary Cushing's disease than in Cushing's syndrome due to other causes. It is not known if the response to oCRF can distinguish pituitary Cushing's disease from those ACTH-secreting bronchial carcinoid tumors that respond to dexamethasone and metyrapone. A case of Cushing's syndrome due to an ACTH-secreting bronchial carcinoid is described in which the responses to dexamethasone, metyrapone, and oCRF were indistinguishable from the responses observed in pituitary Cushing's disease. A bronchial carcinoid tumor should be considered even when responses to dexamethasone, metyrapone, and oCRF suggest pituitary Cushing's disease.
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PMID:Ectopic ACTH syndrome caused by a bronchial carcinoid tumor responsive to dexamethasone, metyrapone, and corticotropin-releasing factor. 284 Aug 23

A male patient with corticotropin-releasing factor (CRF) and adrenocorticotropin (ACTH)-producing syndrome is described. Soon after being referred to us the patient developed pneumonia, anaemia, oedema and respiratory distress, and died on the 24th day after admission. Autopsy and histology revealed that he had a rare type of multiple endocrine neoplasia (type 1 + paraganglioma) with a mediastinal paraganglioma, parathyroidal hyperplasia, pancreatic islet cell adenoma, duodenal multiple carcinoid tumours and adrenocortical nodular hyperplasia. It was not possible to examine the pituitary. The paraganglioma contained a large amount of immunoreactive (IR)-CRF (606 ng/g wet weight), IR-ACTH (59.4 ng/g wet weight), IR-human proopiomelanocortin n-terminal (1-76) peptide (hNT, 156.8 ng/g wet weight) and IR-beta-lipotropin (beta-LPH, 146.9 ng/g wet weight). The major IR-ACTH, beta-LPH and IR-hNT were eluted at ACTH-(1-39), beta-LPH and hNT marker positions, respectively. Big ACTH was not detected. IR-CRF eluted at the human CRF marker position on Sephadex G-75 chromatography and high performance liquid chromatography (HPLC). The IR-CRF fraction from the HPLC showed CRF bioactivity which paralleled that of synthetic human CRF in monolayer cultured rat anterior pituitary cells. Our results suggest that not only ACTH but CRF produced by the paraganglioma was responsible for the patient's Cushing's syndrome.
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PMID:Multiple endocrine neoplasia with Cushing's syndrome due to paraganglioma producing corticotropin-releasing factor and adrenocorticotropin. 287 33


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