Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The glucagonoma syndrome is another of those systemic disorders in which skin manifestations provide a clue to the diagnosis. The patient will most often be a middle-aged woman who has the characteristic, indolent skin lesions in the face of diabetes mellitus and additional features to suggest an occult carcinoma. Marked elevation of the levels of plasma glucagon should confirm the suspicion cure of the skin lesions follows cure of the tumor. Two lines of speculation seem promising. Either the initial event is an overproduction of glucagon and all other observations follow. Or the syndrome is another of the polyendocrine disorders. Cases are still too few to resolve either the pathophysiology, prognosis, or even to guess at the true frequency of the syndrome.
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PMID:The glucagonoma syndrome. 21 45

A 34-year-old man presented with classic glucagonoma syndrome manifested by weight loss, dermatitis, stomatitis, anemia, and mild diabetes mellitus. The diagnosis of glucagonoma was made by light and electron microscopic demonstration of a metastatic alpha cell carcinoma in a liver biopsy specimen. Plasma glucagon concentration was abnormally high. The patient also had symptoms and signs of involvement of the central nervous system. Radionuclide and CAT scans of the brain, negative CSF cytology and myelography excluded the possibility of metastases or other space-occupying lesions. Glucagon was demonstrated in the CSF. We postulate that the neurologic symptoms were due to direct or indirect effect of this hormone on the brain. Following therapy with streptozotocin and 5-fluorouracil, the patient had a subjective and objective clinical and hormonal remission of his disease including amelioration of his neurological impairment.
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PMID:Neurologic involvement in glucagonoma syndrome: response to combination chemotherapy with 5-fluorouracil and streptozotocin. 22 32

A barium enema on a patient with chronic ulcerative colitis demonstrated a stricture with the radiographic characteristics of an annular carcinoma. The "lesion" disappeared following administration of glucagon.
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PMID:Pitfalls to avoid: spasm in ulcerative colitis masquerading as carcinoma. 46 77

Passaging of the mammary aplastic carcinoma several times in diabetic CBA mice induced an extrapancreatic secretion of glucagon. Consequently, the concentration of immunoreactive glucagon was higher in plasma and the tumor tissue extract. After the injection of alloxan, attempts to reduce the level of this hormone in the diabetic mice were unsuccessful. The tumor cells could have been responsible for the secretion of glucagon.
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PMID:Induction of glucagon synthesis in diabetic CBA mice bearing mammary aplastic carcinomas. 48 Mar 74

We compared the maximal calcitonin secretion produced by pentagastrin, calcium, and glucagon for preoperative detection of medullary thyroid carcinoma in four subjects with normal or slightly increased plasma immunoreactive calcitonin (iCT) levels. In each case, pentagastrin administration produced higher peak iCT levels (5- to 36-fold increases over basal) than did calcium infusion (by 1.9- to 10.3-fold) and glucagon administration (by 3.6- to 27.4-fold). These preliminary studies suggest that pentagastrin is an effective agent for use in rapid stimulation tests designed to detectmedullary thyroid carcinoma in asymptomatic patients who have normal basal iCT concentrations.
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PMID:Stimulation tests for diagnosis of medullary thyroid carcinoma. 111 54

Thirty-eight human pancreatic cancer specimens were studied for the reactivity of cancer cells with monoclonal antibodies against insulin, glucagon, somatostatin, pancreatic polypeptide (PP), vasoactive intestinal peptide (VIP), gastrin, calcitonin, and with argyrophilic reactivity. Immunoreactivity with one or several antibodies or argyrophilic reactivity were found in 30 (79%) cases. In 17 cases, the number of endocrine cells was excessive and morphologically consistent with the mixed ductal-islet tumor. Although most immunoreactive cells were located at the base of the malignant glands, some had intraepithelial location and were also present in the invasive portion of cancers, indicating their malignant nature. Endocrine cell proliferation were found in the pancreatic tissue adjacent to the carcinoma in 8 out of 12 specimens examined. In these cases, the immunoreactive cells were either distributed among the acinar cells or ductal cells. More endocrine cells were found in the hyperplastic ducts; however, no correlation was found between the degree of hyperplasia and the occurrence of any type of immunoreactive cells. Although several types of endocrine cells occurred in different pancreatic regions (head, body, and tail), PP cells were restricted to tissues taken from the head of the pancreas. Experimental data and similar observations by other investigators led us to conclude that participation of endocrine cells in ductal-type carcinomas is a general phenomenon and does not justify the classification of these lesions to mixed ductal-islet entity. However, because immunoreactive cells were more common and numerous in well-differentiated carcinomas, they may have some prognostic values.
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PMID:Pancreatic mixed ductal-islet tumors. Is this an entity? 131 18

A total of 24 patients with endocrine neoplasms of the pancreas were clinicopathologically and immunohistochemically studied. They consisted of 18 patients with adenoma and 6 with carcinoma. Of the 24 patients, 13 developed attacks of hypoglycemia due to hyperinsulinemia, and 1 developed an uncontrollable duodenal ulcer caused by the hypersecretion of gastrin, however, the remaining 10 were asymptomatic. No prediction could be made as to the site of origin of the tumors. A clear difference was seen between adenoma and carcinoma in the size of the mass, the mean greatest diameter of the 18 adenoma cases being 1.7 cm, while that of the 6 carcinoma cases was 7.3 cm. One of the 13 insulinomas and a gastrinoma was malignant, while all 24 tumors were positive for neuron-specific enolase. The 13 insulinomas were diffusely positive for insulin and 5 were also shown to be focally immunoreactive for gastrin, with 3 also being immunoreactive for somatostatin and 2 for pancreatic polypeptide. The gastrinoma showed immunoreactivity for somatostatin, insulin, pancreatic polypeptide, and glucagon in addition to a positivity to gastrin. The above findings thus indicate the multiple hormone synthesis of endocrine neoplasms of the pancreas.
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PMID:Endocrine neoplasms of the pancreas: a clinicopathologic study of 24 cases and immunohistochemical remarks. 139 40

Necrolytic migratory erythema is a distinctive cutaneous eruption that occurs in patients with malignant glucagon-secreting tumors of the pancreas. Recognition of this erosive dermatitis as a cutaneous manifestation of an internal malignancy can result in tumor detection and surgical removal prior to metastasis. The case history of a forty-year-old diabetic woman with necrolytic migratory erythema associated with a metastatic glucagon-secreting islet cell tumor of the pancreas is presented. Prior to diagnosis, she had been treated with topical steroids and Mycostatin powder for a recurrent perioral, acral, and intertriginous dermatitis. Because of apparent responsiveness to these medications, the diagnosis of necrolytic migratory erythema was not considered, and the diagnosis of pancreatic carcinoma was delayed for over one year. Wider recognition of the distinctive clinical and histopathologic features of necrolytic migratory erythema should result in earlier detection and possible surgical cure of the associated glucagonoma.
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PMID:Necrolytic migratory erythema: unresolved problems in diagnosis and pathogenesis. A case report and literature review. 156 84

Glucagon and the glucagon-like peptides play important roles in the regulation of glucose homeostasis. Previous studies have demonstrated that approximately 1300 base pairs of rat glucagon gene 5'-flanking sequences direct transgene expression to the pancreas and brain, but not to the intestine, of transgenic mice. These observations suggested that different tissue-specific enhancer elements mediate activation of glucagon gene transcription in the pancreas and intestine. We have now generated mice that express SV40 large T antigen under the control of approximately 2000 base pairs of glucagon gene 5'-flanking sequences. Transgene expression was observed in the brain and pancreas in association with the development of pancreatic endocrine tumors. In contrast to the mice described previously, we also detected transgene expression throughout the gastrointestinal tract in endocrine cells of the stomach and small and large intestine. Focal areas of enteroendocrine cell hyperplasia in the large bowel invariably progressed to invasive and metastasizing plurihormonal endocrine carcinoma, which was clinically and pathologically evident by 4 weeks of age. In contrast, transgene expression in the small bowel and stomach was not associated with progression to either hyperplasia or carcinoma. The results of these studies provide functional evidence for the existence of an upstream cis-acting regulatory domain that directs glucagon gene transcription to the endocrine cells of the intestine in transgenic mice.
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PMID:Glucagon gene 5'-flanking sequences direct expression of simian virus 40 large T antigen to the intestine, producing carcinoma of the large bowel in transgenic mice. 158 47

Apudoma was found in the gall bladder removed in a 76-year-old woman because of the chronic calculous cholecystitis exacerbation. Carcinoid syndrome was absent clinically. Histologically, the tumour was a poorly differentiated carcinoid with areas of small cell and polymorphic carcinoma. Argyrophilic Pasquale reaction in the tumour cells was negative, electron microscopically small neurosecretory granules were found. Numerous ACTH-reactive cells and single serotonin-reactive cells were revealed in the tumour parenchyma by means of immunohistochemical PAP-method using antibodies against ACTH, serotonin, calcitonin, somatostatin, insulin, glucagon, P-substance. Focal hyperplasia and intestinal metaplasia of epithelium with the increase of the number of argyrophilic, ACTH-reactive cells were observed outside the tumour.
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PMID:[A poorly differentiated apudoma of the gallbladder]. 170 8


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