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)

To study the relationship between null cell adenomas, oncocytomas and gonadotroph adenomas, we analyzed 32 surgically removed formalin-fixed paraffin-embedded pituitary tumors for the expression of pituitary hormone messenger RNAs (mRNAs) by in situ hybridization (ISH). Most tumors were also analyzed for chromogranin A mRNA. To identify the cell type constituting the tumors and to assess hormone content, all tumors were investigated by histology, transmission electron microscopy and immunohistochemistry. Most null cell adenomas (6/11) and gonadotroph adenomas (9/10) expressed the mRNAs for alpha-subunit of glycoprotein hormones whereas only 2/11 oncocytomas expressed alpha-subunit mRNA. FSH beta and/or LH beta mRNA were present in most null cell and gonadotroph adenomas but only in a few oncocytomas. Prolactin (PRL) mRNA was detected in two null cell tumors and in one gonadotroph adenoma, whereas GH and POMC mRNA were present in one null cell adenoma. Chromogranin A mRNA, which codes for the major secretory granule protein, was present in 25/26 tumors including all tumors that were negative for pituitary hormone mRNAs, indicating adequate preservation of specific mRNA transcripts in the paraffin-embedded sections of tumor cells. These results indicate that null cell adenomas and gonadotroph adenomas are closely related neoplasms and that oncocytomas may represent a functionally defective form of null cell adenoma characterized by mitochondrial abundance, which has retained the capacity to synthesize the major secretory granule protein chromogranin A. Although the cytogenesis of null cell adenomas and oncocytomas is not clear, it can be suggested that these two tumor types are derived from a pluripotential precursor cell that is capable of undergoing multidirectional differentiation and synthesizing various hormones, mainly glycoproteins.
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PMID:Analysis of pituitary hormones and chromogranin A mRNAs in null cell adenomas, oncocytomas, and gonadotroph adenomas by in situ hybridization. 165 18

Routinely processed parathyroid tissues from 26 cases with primary hyperparathyroidism (19 adenomas, 7 multiglandular hyperplasia) and 8 normal human parathyroid glands were investigated with antibodies against chromogranin A and B and parathyroid hormone (PTH). Normal parathyroids were immunohistochemically positive for PTH and chromogranin A but negative for chromogranin B. Hyperplastic glands showed a focal staining for PTH and chromogranin A without correlation of the staining pattern on serial sections. Adenomas were either uniformly positive for both PTH and chromogranin A or showed a staining pattern similar to that seen in hyperplastic glands. Focal chromogranin B positivity (less than 10% of cells) was found in 3 cases (1 hyperplastic gland and 2 cases of parathyroid adenoma with an immunohistochemical staining pattern similar to hyperplastic glands). Our immunohistochemical results may support previously published findings that most parathyroid adenomas are monoclonal neoplasms whereas hyperplastic glands are of polyclonal origin.
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PMID:Chromogranin A and B in parathyroid tissue of cases of primary hyperparathyroidism: an immunohistochemical study. 202 50

The ultrastructural localization of chromogranin A (Chr A) was studied in eleven neoplasias of the diffuse neuroendocrine system (3 pancreatic islet-cell tumours, 1 medullary carcinoma of the thyroid, 1 large bowel and 1 small bowel carcinoid tumours, 2 carcinoid tumours of the lung, 1 adenoma of the parathyroid gland, 2 pheochromocytomas of the adrenal gland). On account of the great influence of the technical treatment of the samples on the immunolocalization of Chr A, the effect of the following variables was studied in a case of pheochromocytoma: fixation in glutaraldehyde versus paraformaldehyde, postfixation in osmium tetroxide versus omission, embedding in epoxy resin versus acrylic resin. The method of choice for the better preservation of the antigenic character of the tissue was found to be fixation in 4% paraformaldehyde, omission of osmium postfixation and embedding in LRWhite acrylic resin; by this procedure we were able to find Chr A in the neurosecretory granules of all the studied cases, using three commercially available antibodies directed against Chr A. These findings further confirm that Chr A is a reliable marker for the study of neuroendocrine neoplasias by electron microscopy.
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PMID:Chromogranin A as a marker of neuroendocrine histogenesis of tumours: an immunoelectron microscopic study with considerations about the influence of fixation and embedding media on immunolabelling. 222 1

Dopamine receptors were analyzed in plasma membranes from five null cell adenomas and five normal human pituitary tissues by [3H]spiperone binding. One prolactin (PRL)-producing, one growth hormone (GH)-producing, and an adrenocorticotropic (ACTH)-producing adenoma were also analyzed for dopamine receptors. Immunohistochemical staining showed that all null cell adenomas were positive for chromogranin A, while 20 to 30% of cells in each normal pituitary stained for this marker. The dissociation constant (Kd) and maximal binding capacity (Bmax) were 1.07 +/- 0.49 nM and 148 +/- 34 fmol/mg protein for null cell adenomas and 1.23 +/- 0.20 nM and 107 +/- 21 fmol/mg protein for normal pituitary tissues. The one PRL adenoma had a similar Kd but had a 5.6-fold higher Bmax than the mean Bmax for the null cell adenomas. These results indicate that immunohistochemically characterized null cell adenomas as well as normal pituitaries express dopamine receptors, but that the binding sites in null cell adenomas are much less those in PRL-secreting adenomas.
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PMID:Dopamine receptors in immunohistochemically characterized null cell adenomas and normal human pituitaries. 246 83

Chromogranin A, the protein that is co-stored and co-released with catecholamines from the adrenal medulla, has recently been identified in a variety of human endocrine tissues, both normal and neoplastic. We investigated the secretion of chromogranin A by peptide hormone-producing human tumors in studies of patients with the following neoplastic disorders: pheochromocytoma, parathyroid adenoma, primary parathyroid hyperplasia, medullary thyroid carcinoma, thyroidal C-cell hyperplasia, carcinoid tumor, oat-cell lung carcinoma, pancreatic islet-cell tumor, and aortic-body tumor. All these patient groups had elevated concentrations of plasma chromogranin A. We distinguished different forms of immunoreactive plasma chromogranin A by size with the use of gel filtration. Plasma chromogranin A levels were not elevated in patients with diverse "control" conditions--both benign and malignant and both endocrine and nonendocrine--in which peptide hormones are not produced. The sensitivity and specificity of plasma chromogranin A elevations in the diagnosis of peptide-producing endocrine neoplasms were 81 and 100 percent, respectively. The elevation of plasma chromogranin A in our subjects suggests that their neoplasms co-release chromogranin A along with the usual resident hormone of the tumor, that these neoplasms could be characterized as "chromograninomas," and that measurement of plasma chromogranin A may be a useful diagnostic procedure in subjects with endocrine tumors, especially multiple endocrine neoplasia.
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PMID:Secretion of chromogranin A by peptide-producing endocrine neoplasms. 300 86

Chromogranin A, the major soluble protein costored and coreleased by exocytosis with catecholamines from the adrenal medulla, has recently been detected in several bovine polypeptide hormone producing tissues. We therefore searched for chromogranin, by immunohistology, in human polypeptide hormone producing tumors as well as normal human endocrine tissues. The chromogranin A antigen was purified from catecholamine storage vesicles of human pheochromocytoma, to which rabbit antisera were developed, allowing immunohistologic studies by the indirect rabbit anti-peroxidase technique. Specific chromogranin staining was noted in all polypeptide hormone producing human tumors studied (pheochromocytoma chromaffin cells, n = 3; medullary thyroid carcinoma parafollicular C cells, n = 2; thyroidal C cell hyperplasia cells, n = 1; parathyroid adenoma chief cells, n = 1; pancreatic islet cell tumor islet cells, n = 1; oat cell carcinoma cell line M-103) as well as in all normal polypeptide hormone producing tissues (adrenal medulla chromaffin cells, parathyroid chief cells, thyroid parafollicular C cells, pancreatic islet cells, gut enteroendocrine cells, and anterior pituitary cells). Chromogranin may have a widespread distribution in human polypeptide hormone producing tissues, and may be a useful histologic marker for peptide producing tumors.
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PMID:Immunoreactive human chromogranin A in diverse polypeptide hormone producing human tumors and normal endocrine tissues. 635 25

Fifteen adenomatous parathyroid glands obtained from 15 patients with primary hyperparathyroidism were examined both pathologically and immunohistochemically and connected with the clinical data for each patient. Four consecutive sections of the largest section surface of each resected adenomatous parathyroid gland were utilized for 4 kinds of stains, that is, hematoxylin-eosin, Grimelius and the immunohistochemical stains for parathyroid hormone (PTH) and chromogranin A. The results were as follows: (1) The large adenomatous parathyroid glands showed strong reactions to PTH as well as chromogranin A and Grimelius. On the other hand, the parathyroid adenoma obtained from a 9-year-old boy with hypercalcemic crisis showed almost no stain-positive cells for both PTH and chromogranin A. It is assumed that the former phenomenon reflects a substantial storage of secretory granules, while the latter reflects exhaustion of these granules. (2) The normal parathyroid cells in the neoplastic parathyroid glands generally showed stronger reactions to PTH and chromogranin A than neoplastic parathyroid cells. This suggests that normal cells in the neoplastic parathyroid glands may have their release of PTH rather than its synthesis suppressed, and also might support the hypothesis of some authors that chromogranin A or SP-I might contribute to stabilization of PTH or the secretory vesicle.
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PMID:Light microscopical immunohistochemical study on parathyroid adenoma in primary hyperparathyroidism. 751 33

Two hundred and nineteen (33 GH, 21 GH-PRL, 38 PRL, 16 ACTH, 1 TSH cell functioning and 38 FSH-LH, 17 alpha-chain, 8 mixed, 27 minimal glycoprotein--MIN-GLYC--, 11 small argyrophil granule--SAG--, 4 silent TSH-sTSH--and 5 silent ACTH-sACTH--cell nonfunctioning) adenomas were investigated immunohistochemically with antibodies against ACTH, GH, PRL, TSH, FSH, LH alpha-hCG, chromogranin A (CgA) and chromogranin B (CgB). For immunostaining of CgB a novel monoclonal (B 11) antibody was employed. All types of adenomas were positive for CgB. CgA was widely expressed in nonfunctioning FSH-LH, MIN-GLYC, SAG, MIXED, alpha-chain adenomas and in the single TSH cell functioning adenoma. CgA was lacking both in PRL and ACTH functioning adenomas and was poorly expressed in GH and GH-PRL functioning adenomas. The distribution of Grimelius' silver paralleled that of CgA-IR, but not that of CgB-IR. We conclude that: 1) CgB may be considered as an universal granular marker for pituitary adenomas, 2) CgA is an important marker for nonfunctioning adenomas, 3) the pattern of distribution of CgA and CgB for most nonfunctioning ("null cell" according to Kovacs et al.) adenomas favors their origin from glycoprotein producing (FSH/LH, TSH) cells.
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PMID:Different expression of chromogranin A and chromogranin B in various types of pituitary adenomas. 839 20

Of 1,106 New World primates necropsied from the National Zoological Park (Washington, D.C.) and the Department of Comparative Pathology, Johns Hopkins University School of Medicine (Baltimore, Maryland) 22 (1.9%) animals were identified with 27 neoplasms. Of this group, nine animals (two females, seven males) had a total of 13 endocrine neoplasms. All animals were adults, with an age range of 2.7-25 years (average, 12.1 years). Seven were Callitrichidae and two were Cebidae. The adrenal gland was the most affected organ, with seven (53.8%) neoplasms, followed by the pituitary and thyroid gland with two (15.4%) cases each, and the pancreas and parathyroid gland with one tumor (7.7%) each. All neoplastic disorders were benign. Immunocytochemistry assays for growth hormone, adrenocorticotropic hormone, prolactin, follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, and chromogranin A were performed on two pituitary neoplasms. Pheochromocytoma was the most frequent neoplasm, representing 5 (38.4%) of the 13 neoplasms. The remaining were thyroid cystadenoma (two, 15.4%), corticotrophic cell pituitary adenoma (two, 15.4%), adrenal ganglioneuroma (one, 7.7%), adrenal cortical adenoma (one, 7.7%), parathyroid chief-cell adenoma (one, 7.7%), and pancreatic islet-cell adenoma (one, 7.7%).
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PMID:Endocrine neoplasia in New World primates. 874 Sep 50

We report three cases of intrathyroidal paraganglioma. The patients were adult women without significant personal or family histories that presented with an asymptomatic thyroid nodule. The tumors were single, well-circumscribed solid masses, 2 cm in greatest diameter, located within one thyroid lobe. Microscopically, they were encapsulated and showed the typical nesting (Zellballen) pattern of paraganglioma in other sites. Two of the tumors were composed of small- to medium-sized cells with granular amphophilic cytoplasm, and the third consisted of relatively large cells having a similar staining quality. Immunohistochemically, all tumors showed positivity for neuron-specific enolase, chromogranin A, and synaptophysin. S-100 protein-positive sustentacular cells were demonstrated in each case. Negative staining for epithelial markers, thyroglobulin, carcinoembryonic antigen, calcitonin, calcitonin gene-related peptide, serotonin, vimentin, and Congo red excluded other tumors that were considered in the differential diagnosis, such as medullary carcinoma, hyalinizing trabecular adenoma, atypical follicular adenoma, Hurthle-cell neoplasm, and metastatic carcinoid tumor. The patients were alive and well without evidence of recurrent disease at the time of the last follow-up. The previous literature on these tumors is discussed. We conclude that intrathyroidal paraganglioma exists and that this tumor can be distinguished from other similar-appearing neoplasms in this organ.
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PMID:Thyroid paraganglioma: a clinicopathologic and immunohistochemical study of three cases. 923 30


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