Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systematic detection of endocrine cells was performed in two genital tracts from patients with Peutz-Jeghers syndrome (PJS). These tissues proved to be particularly rich in endocrine cells. The specialized cells were distributed in the cervix and fallopian tubes. In the cervix, they were confined to remarkable mucinous tumors related to "adenoma malignum." Serotonin, somatostatin, gastrin, and pancreatic polypeptide immunoreactive cells were characterized. In fallopian tubes, serotonin-storing cells and somatostatin cells were detected respectively among normal-appearing and mucinous areas of tubal epithelium; in addition, serotonin-storing cells were found in many mesonephric rests. This strongly contrasts with the usual paucity of endocrine cells in the female genital tract. However, none of the findings mentioned was really specific of PJS. In particular, endocrine cells seem to be an integral constituent of adenoma malignum, with or without PJS. These findings suggest a disturbance of tissular differentiation.
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PMID:Female genital tract and Peutz-Jeghers syndrome: an immunohistochemical study. 390 86

In a series of 44 patients with pernicious anemia examined by gastroscopy, three cases of gastric carcinoids were found. During the same ten-year period about 11,000 gastroscopies were performed on patients not suffering from pernicious anemia, and only one case of gastric carcinoid was detected. In two of the cases no endoscopic lesion was seen and the carcinoid was detectable only at histological examination, while in one case an unusual combination of carcinoid tumor and tubular adenoma in the same polyp was found. Most of the carcinoids arose in atrophic body mucosa, but in one case the mucosa around the carcinoid showed antral properties. One patient had slightly elevated values of pancreatic polypeptide, while no hormonal activity was found in others. No growth or spread of the carcinoid was observed during follow-up. It is suggested that the same pathogenetic factors may operate in the genesis of gastric carcinoid and gastric carcinoma in patients with pernicious anemia.
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PMID:Gastric carcinoids with minimal or no macroscopic lesion in patients with pernicious anemia. 400 65

An encapsulated, compact-type islet cell adenoma of the pancreas, found in a newborn infant with hyperinsulinemic hypoglycemia, was investigated by conventional histology and immunofluorescence. Although the histologic structure of the tumor was indistinguishable from that of most islet cell tumors of adults, immunofluorescence revealed that the four islet cell hormones (insulin, glucagon, somatostatin, and pancreatic polypeptide) were all present in the tumor. They were stored in different cells that showed the same spatial distribution usually seen in normal islets. We conclude that neonatal islet cell adenoma can be distinguished from those of adults on the basis of the content and topographic distribution of their constituent endocrine cells.
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PMID:Neonatal islet cell adenoma: a distinct type of islet cell tumor? 610 Aug 86

Percutaneous transhepatic sampling of blood in the portal venous system (TPVS) was used to; (1) localize hormone secreting tumors and help in differentiating tumors from diffuse disease (nesideoblastosis and hyperplasia with adenomata) in 9 patients with fasting hypoglycemia and hyperinsulinism, and (2) study the concentration an distribution of the immunoreactive peptides: insulin (IRI), gastrin (IG), glucagon (IRG), pancreatic polypeptide (hPP), and somatostatin (SRIF-LI), in the venous drainage of the uninvolved portion of the pancreas and GI tract. Localized elevations of IRI (64-920 microunits/ml) predicted tumor localization in 6 patients with single tumors that were not demonstrable angiographically. In one patient with nesideoblastosis and another with islet cell hyperplasia with adenoma, elevated IRI concentrations at multiple locations suggested a diffuse or multicentric process. Elevations of SRIF-LI in the same region as IRI elevations in one patient and of IRG in another patient suggested that these tumor produced two hormones. Some problems in the interpretation of portal venous insulin concentrations are discussed. The locations of maximum portal venous system plasma concentrations and portal-arterial gradients (mean +/- SE pg/ml) in five patients with small single insulinomas were: IG, gastrocolic trunk (126 +/- 27, 46 +/- 22); IRG, proximal splenic vein (130 +/- 30, 47 +/- 13) and gastrocolic trunk (131 +/- 23, 60 +/- 13); hPP, portal vein (164 +/- 48, 49 +/- 22); SRIF-LI, superior mesenteric vein (186 +/- 50, 57 +/- 20) and gastrocolic trunk (178 +/- 59, 55 +/- 21). It is concluded; (1) TPVS can be used successfully to localize single insulin-secreting tumors of the pancreas and to help distinguish them from diffuse disease but problems in such differentiation do occur, (2) circulating SRIF-LI and IRG are derived from both the pancreas and the gut, IG predominantly from the proximal gut and hPP from the head of the pancreas, and (3) The data provide new information for the interpretation of portal insulin concentrations in patients with organic hyperinsulinism and of hormone concentrations for localization of peptide-producing tumors of the pancreas other than insulinomas.
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PMID:Gastrointestinal/pancreatic hormone concentrations in the portal venous system of nine patients with organic hyperinsulinism. 611 52

Circulating human pancreatic polypeptide (hPP) concentrations in the plasma of 61 patients were determined by radioimmunoassay and compared with concentrations in normal age-matched subjects to assess the role of plasma hPP in diagnosis and detection of pathologic dysplasias in endocrinopathies. Basal fasting plasma hPP concentrations greater than 3.0 times normal values were found in six of six patients with multiple endocrine adenopathy syndrome, type I (MEA I) who had islet cell tumors that contained hPP and in only three of 15 nonfamilial patients with sporadic islet cell tumors. An exaggerated plasma hPP response to meal stimulation that exceeded greater than 4.5 times the basal value was found in 15 of 18 patients with MEA I, which indicated the presence of endocrine cell hyperplasia as the underlying genetic trait. The abnormal plasma hPP response to meal stimulation correlated most strongly with islet cell hyperplasia in both the genetic and sporadic endocrinopathies and to some extent with antral G cell hyperplasia. In patients with primary hyperparathyroidism, an exaggerated plasma hPP response to meal stimulation is highly indicative of genetic parathyroid hyperplasia in MEA I and not of sporadic parathyroid adenoma. Informed consent was obtained from all patients who were subjects of these investigations.
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PMID:Pancreatic polypeptide update: its roles in detection of the trait for multiple endocrine adenopathy syndrome, type I and pancreatic polypeptide-secreting tumors. 613 85

In a pancreatic adenoma approximately 78.7% of the endocrine cells reacted specifically with antisera to neurotensin, 17.5% to gastrin, 2.8% to pancreatic polypeptide, and 1% to glucagon. The electron microscope revealed that the majority of the endocrine cells were N-cells--morphologically similar to the ileal N-cells which are known to represent the neurotensin-producing cells. Neurotensin was extracted from the tumor and identified by Sephadex, ion-exchange, and high-pressure liquid chromatography. Gastrin, pancreatic polypeptide, and glucagon cells were also identified by the electron microscope; the peptides were extracted and demonstrated by chromatography. The serum concentrations of these hormones were elevated. After total gastrectomy which was necessary because of Zollinger-Ellison syndrome, a jejunoesophageal alkaline reflux, reaching the upper esophagus appeared. As intravenous infusion of synthetic neurotensin in rats caused an increase of luminal enteric pressure, it is suggested that severe jejunoesophageal reflux after gastrectomy may be a clinical feature of a neurotensinoma.
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PMID:A multihormonal tumor of the pancreas producing neurotensin. 730 61

Prolactinoma is the most common type of primary pituitary tumors. It occurs more frequently in women than in men. Dopaminergic agonists are effective in the shrinkage of prolactin-secreting pituitary tumor and are preferred in some patients. However, pituitary radiotherapy may enable the long-term removal of prolactin-secreting tumor cells. Recent evidence suggests that prolactinoma is a heterogeneous disorder with complicated and multifactorial etiology and pathogenesis. Apparently, a thorough understanding of prolactinoma tumorigenesis would be important. To facilitate investigations on tumorigenesis of prolactinoma, animal models for prolactinomas have been developed. These models have expedited our progress in the recent years. Many researchers consider the F(344) rat to be the most sensitive strain of rats to estrogen (E(2))-induced prolactinoma formation. Nonetheless, E(2) treatment for 60 days also induces the formation of pituitary prolactin-secreting adenoma in male Sprague-Dawley (SD) rats. Evidently, the SD rat is also a good animal for prolactinoma investigations. Following E(2) implantation, prolactinomas developed in the eutopic adenohypophysis in situ and/or ectopic pituitary grafted under the renal capsule in SD rats. These observations favor the hypothesis that prolactinoma growth is the result of pathological changes in the adenohypophysis and/or hypothalamus. In the latter case, abnormal release of hypothalamic dopamine, GABA, or brain-gut peptides (such as cholecystokinin, vasoactive intestinal polypeptide, galanin, angiotensin, opioid peptide, gastrin, gastrin-releasing peptide, pancreatic polypeptide, and adrenocorticotropic hormone) results in some of the pathological changes that may lead to hyperprolactinemia and/or prolactinoma development. Dysregulation of prolactin synthesis and secretion may be the result of prolactin gene modulation. In E(2)-induced rat prolactinomas, prolactin mRNA contents and the expression of some proto-oncogenes, e.g. c-myc and c-ras, TGFalpha and TGFbeta1 mRNA were significantly changed. The above findings are consistent with results in human prolactinoma development. In addition, in rats abnormal expression of the prolactin gene was correlated with hypomethylated status of CpG sites in exons 1, 2 and 4 of the prolactin gene, as well as the increase in hypersensitive sites to DNase 1 in the encoding region of the prolactin gene. In E(2)-treated rats, a point mutation with a base substitution from cytidine (C) to adenine (A) was found at the -36-bp site of the proximal promoter of the prolactin gene in eutopic pituitary prolactinomas, but no change was observed in the same sequence of the prolactin gene in ectopic prolactinoma. The association of a base substitution with the hyperexpression of the prolactin gene in eutopic prolactinomas suggests that different mechanisms may mediate the formation of eutopic and ectopic prolactin-secreting tumors. Melatonin decreases the expression of the prolactin gene in vitro suggesting that this pineal hormone may be a potential anticarcinogen in vivo. It has also been shown that MT(2) (Mel(1b)) melatonin receptors are expressed in anterior pituitary cells. The use of melatonin as a preventive or therapeutic drug for prolactinomas should be further investigated. In summary, improved knowledge on tumorigenesis of prolactinomas, especially in the rat model, was noted. These E(2)-induced rat prolactinoma models would facilitate future investigations, and expected results shall be fruitful and exciting for the development of future drug designs for the prevention and/or treatment of prolactin-secreting pituitary tumors.
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PMID:Pituitary prolactin-secreting tumor formation: recent developments. 1068 32

Carcinoid tumors and adenomas of the middle ear are rare neoplasms of indeterminate relationship to one another. Indeed, the literature is devoid of a large comprehensive series that evaluates the clinical, histologic, and immunophenotypic features of these tumors and their potential relationship. Forty-eight cases of middle ear adenoma between 1970 and 1995 were identified in the files of the Armed Forces Institute of Pathology. All cases were evaluated for cytomorphology and architectural pattern, in addition to their reactivity with various immunohistochemical reagents. Clinical follow-up was also obtained. A comprehensive review of the literature was performed with an eye toward correlating any distinct differences or similarities between carcinoid tumors and adenomas of the middle ear. The patients included 21 women and 27 men, aged 20 to 80 years (mean, 45.0 y). Patients experienced hearing loss, mass, and/or pain for a mean duration of 1.7 years. The mean tumor size was 0.8 cm, with six tumors extending beyond the middle ear. Histologically, the tumors were moderately cellular and unencapsulated, arranged in glandular, trabecular, and solid patterns composed of small cells with "salt and pepper" nuclear chromatin distribution. The tumor cells were immunoreactive with keratin, keratin 7, chromogranin, and human pancreatic polypeptide. All patients had surgery. No patients died with their disease (mean follow-up, 15.7 y). Eight patients developed recurrences that were treated surgically and were without evidence of disease at last follow-up (mean, 15.1 y). Our study and the review of the literature showed adenomas and carcinoid tumors of the middle ear to be essentially indistinguishable benign tumors. Middle ear adenoma most correctly describes their morphologic features and clinical behavior, although neuroendocrine adenoma of the middle ear may be a more accurate designation.
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PMID:Adenoma versus carcinoid tumor of the middle ear: a study of 48 cases and review of the literature. 1201 Dec 60

The clinical and histochemical examination of hormone-producing serous cystadenomas of the pancreas are presented. The study material was obtained from five female patients. The patients underwent diagnostic examinations, including ultrasonography, computer tomography (CT), magnetic resonance imaging (MRI) and Doppler ultrasonography examination of abdomen. In all cases the presence of serous cystadenoma of pancreas was detected in the histopathologically verified sections. The test applied to immunohistochemically localize paraffin-embedded sections of neoplastic tissues of the pancreas was the LSAB2-HRP test using monoclonal antibodies against epithelial membrane antigen (EMA), carcinoembryonic antigen (CEA), synaptophysin, p53 and polyclonal antibodies against insulin, glucagon, somatostatin and pancreatic polypeptide. In one patient, ultrasonography revealed an irregular space filled with fluid resembling a multicellular cystic lesion. The Doppler ultrasonography examination showed a pathologically vascularized focus in the pancreatic head. In the adenoma sections of this patient, the immunohistochemical techniques revealed a strong positive somatostatin, pancreatic polypeptide and synaptophysin expression in the lining epithelium of neoplastic cysts.
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PMID:Hormone-producing serous cystadenoma of the pancreas. 1716 18


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