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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pituitary adenomas that are characterized by the absence of a particular clinical syndrome and the absence of excessive hormone secretion have been classified as nonfunctioning adenomas. Recent development of immunohistochemical analysis and hormonal assay have suggested that many of these tumors have function to secret the gonadotropin subunits. A novel procedure biotin amplification in immunohistochemistry, catalyzed signal amplification (CSA) has been reported recently. In this study, the authors applied this new method to tissues from 50 cases of clinically nonfunctioning adenomas. These cases had no evidence of endocrinological signs by hormone secretion. When the CSA system was applied in normal pituitary gland, each of subunits was positive even when the antibody was diluted 1:1,000,000, which is 1,000 folds of standard indirect immunoperoxidase method. Immunohistochemical staining by indirect immunohistochemical method revealed that all 50 adenomas were negative for all the anterior hormones, including growth hormone (GH), prolactin (PRL), adrenocorticotropic hormone (ACTH), beta-subunit of luteinizing hormone (LH beta), follicle-stimulating hormone (FSH beta), thyroid stimulating hormone (TSH beta), and a-subunit of glycoprotein (alpha SU). Using avidin-biotin complex (ABC) method, two cases were positive for FSH beta and four cases were positive for alpha SU, respectively, and the immunopositivities were observed weakly in scattered cells. By CSA system, 26 cases of 50 nonfunctioning adenoma were positive for FSH beta, 16 cases were positive for LH beta, and 29 cases were positive for alpha SU, respectively. The immunoreactivities were clearly observed in cytoplasm of many adenoma cells. This amplification procedure provides a means of greatly increasing the sensitivity of the immunohistochemistry including subunits of glycoproteins that are difficult to detect by previous indirect immunoperoxidase method or ABC method. This amplification procedure provides a great increase in the sensitivity of the immunohistochemistry for the detection of gonadotropin subunits and suggest that significant proportion of the nonfunctioning adenomas are gonadotropin subunit producing adenomas.
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PMID:Application of catalyzed signal amplification in immunodetection of gonadotropin subunits in clinically nonfunctioning pituitary adenomas. 870 26

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

Somatotroph adenomas often secrete prolactin (PRL) besides growth hormone (GH) and are sometimes immunostained for other anterior pituitary hormones or their subunits, such as thyroid-stimulating hormone (TSH) beta-subunit and glycoprotein hormone alpha-subunit (alpha SU). However, somatotroph adenomas showing hypersecretion of adrenocorticotropic hormone (ACTH) are extremely rare. There have been, to our knowledge, only five published reports on somatotroph adenomas accompanied by excessive ACTH secretion. Here we report a case of intracavernously invading somatotroph macro-adenoma with high serum GH, PRL, and ACTH levels. We examined the case using immunohistochemistry (IHC), in situ hybridization (ISH), and cell culture, and confirmed GH, PRL, and ACTH, as well as alpha SU, production, and the expression of Pit-1 protein by the adenoma, which is known as a transcriptional factor for GH, PRL, and TSH, not for ACTH. Therefore, the presence of unknown transcriptional factor other than Pit-1, common to GH, PRL, and ACTH, may be speculated to be expressed in this adenoma. In our previous study, we had found plurihormonal mRNA expression, especially for ACTH, the beta-subunit of follicle-stimulating hormone and luteinizing hormone in some somatotroph adenomas, using non-radio-isotopic ISH, and suggested that these adenomas might be derived from plurihormonal primordial stem cells. Our present case is significant from the viewpoint of histogenesis of pituitary adenomas, because it further supports the cell origin of somatotroph adenomas from plurihormonal primordial stem cells, and moreover it suggests the presence of unknown transcriptional factor other than Pit-1, common to GH, PRL, and ACTH.
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PMID:A case of pituitary somatotroph adenoma with concomitant secretion of growth hormone, prolactin, and adrenocorticotropic hormone--an adenoma derived from primordial stem cell, studied by immunohistochemistry, in situ hybridization, and cell culture. 889 Sep 99

Retinoid X receptors (RXRs) are transcriptional factors that belong to the steroid/thyroid hormone receptor superfamily. There are 3 RXR isoforms-alpha, beta, gamma-known to bind 9-cis-retinoic acid as their ligand. The expression of RXRs in human pituitary glands and pituitary adenomas has not been extensively investigated. To determine whether specific RXR isoforms may play roles in the state of differentiation of pituitary adenomas, we have investigated the immunohistochemical expression of RXR alpha and RXR gamma in 6 nontumorous pituitaries and in 60 different pituitary adenomas using isoform-specific antibodies. In the nontumorous pituitaries. RXR alpha was expressed in the nuclei of almost all cells, while RXR gamma was only expressed in thyrotropin (TSH) cells and in some cells positive for growth hormone (GH) and glycoprotein alpha-subunit (alpha SU) but not in luteinizing hormone (LH) beta-subunit, follicle-stimulating hormone (FSH) beta-subunit, prolactin (PRL) or adrenocorticotropin (ACTH) cells by double immunostaining. All 60 adenomas were RXR alpha positive, and 39 of 60 adenomas (65%) were positive for RXR gamma. The incidence of RXR gamma immunoreactivity in the different adenoma types was: 13 of 16 GH-producing adenomas (81.3%), 9 of 14 PRL-secreting adenomas (64.3%), 6 of 6 TSH-secreting adenomas (100%), 2 of 5 ACTH-secreting adenomas (40%) and 9 of 19 nonfunctioning adenomas (47.4%) including immunohistochemically gonadotropin-subunit-positive adenomas. The colocalization of RXR gamma with the TSH beta subunit, GH and alpha SU in the same adenoma cells was frequently observed, and sometimes RXR gamma was colocalized with PRL, ACTH, FSH beta or LH beta as shown by double immunostaining. We conclude that RXR alpha is expressed in both human pituitaries and pituitary adenomas. In contrast, RXR gamma is expressed more broadly in pituitary adenomas than in normal pituitaries and thus may play a role in the differentiation-specific cell types in the human pituitary both under physiological and pathological conditions.
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PMID:Immunohistochemical expression of retinoid X receptor isoforms in human pituitaries and pituitary adenomas. 914 2

The growth hormone (GH)-releasing hormone receptor (GHRH-R) has been recently cloned and found to be a member of a new family of seven transmembrane receptors that includes secretin, vasoactive intestinal peptide, calcitonin, and corticotropin-releasing factor. GHRH-R mRNA has been demonstrated by Northern blot analyses to be present specifically in the anterior pituitary gland. To determine the precise cellular localization of this receptor in normal anterior pituitary and pituitary adenomas, GHRH-R mRNA was analyzed in 2 normal human pituitary glands and 16 human pituitary adenomas using in situ hybridization. GHRH-R was specifically localized in somatotroph cells in the normal pituitary. In the adenomas, all GH-producing adenomas originating from acromegalic patients demonstrated up-regulation of GHRH-R mRNA when compared with levels in the normal pituitary. Only one of five clinically nonfunctioning adenomas, a gonadotroph luteinizing hormone/follicle-stimulating hormone-positive adenoma, exhibited up-regulation of this receptor message. Adrenocorticotrophic hormone-secreting and prolactin-secreting adenomas did not express GHRH-R message. In summary, GHRH-R is specifically expressed in somatotrophs and GH-producing adenomas, suggesting that GHRH-R may influence GH release in adenomas similar to this receptor's actions in the normal somatotrophs and may be involved in the growth of GH-secreting adenomas.
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PMID:Growth hormone-releasing hormone receptor mRNA in acromegalic pituitary tumors. 917 81

Adenomas causing acromegaly represent at least a quarter of pituitary adenomas. We studied 12 patients presenting with active acromegaly due to a pituitary adenoma with a 1.5 T superconductive MRI unit. All had T1-weighted sagittal and coronal sections before and after Gd-DTPA; six had coronal T2-weighted images. Surgical correlation was obtained in seven patients. Histologically, there were eight growth hormone (GH)-secreting and three mixed [GH and prolactin (PRL) secreting] adenomas, and one secreting GH, PRL and follicle-stimulating hormone. Macroadenomas (10) were more frequent than microadenomas (2). No correlation was found between serum GH and tumour size. There were nine adenomas in the lateral part of the pituitary gland; seven showed lateral or infrasellar invasion. Homogeneous, isointense signal on T1- and T2-weighted images was observed in six cases. Heterogeneous adenomas had cystic or necrotic components.
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PMID:MRI of pituitary adenomas in acromegaly. 922 16

To elucidate the contribution of growth factors to the development, growth and behavior of human pituitary adenomas, the authors used competitive reverse transcription-polymerase chain reactions to quantify expression of mRNAs for growth factors extracted from pituitary adenomas. As previously diagnosed by endocrinologic evaluation, the pituitary adenomas in this study consisted of six prolactin-producing, six growth hormone (GH)-producing, four follicle-stimulating hormone producing and six nonfunctioning adenomas. The mRNAs examined included those for platelet-derived growth factor (PDGF) B-chain, transforming growth factor (TGF)-beta1, epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and insulin-like growth factor (IGF)-I and -II; proliferating cell nuclear antigen (PCNA) as an indicator of cell proliferation; and pituitary-specific transcription factor-1 (Pit-1) which is a nuclear transcription factor expressed in the anterior pituitary. All factors except the last were expressed in all adenomas, and expression of PDGF B-chain, TGF-beta1, EGF, bFGF and IGF-II did not differ between the four adenoma varieties. Pit-1 was expressed only in GH- and prolactin-producing adenomas. PCNA expression also showed no differences. However, IGF-I mRNA in GH-producing adenomas was significantly lower than in prolactin-producing and nonfunctioning adenomas despite high serum IGF-I levels (1121+/-253 ng/ml). The analysis on IGF-I receptor mRNA was significantly lowered in GH-producing adenoma compared with the other types of adenoma. These findings suggest that the attenuation of negative feedback through the pituitary GH-IGF-I axis may be involved in development of GH-producing adenoma.
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PMID:Quantitative analysis of growth-related factors in human pituitary adenomas. Lowered insulin-like growth factor-I and its receptor mRNA in growth hormone-producing adenomas. 1049 42

Two of 420 patients with pituitary adenoma who underwent operation from 1989 to 1997 had thyroid stimulating hormone (TSH) producing adenoma. We investigated these TSH cell adenomas with immunohistochemical and ultrastructural methods and compared their ultrastructural features with brefeldin A (BFA, 0.5 mg/ml) treated pituitary adenoma cells. BFA-treated pituitary adenomas include a prolactin (PRL) cell adenoma, a growth hormone (GH) cell adenoma, an adrenocorticotropic hormone (ACTH) cell adenoma, a gonadotroph adenoma, and a plurihormonal adenoma. Immunohistochemical staining disclosed that one of the TSH cell adenomas produced only TSH-beta and that another produces both TSH-beta and FSH-beta. Ultrastructural analysis showed the abundance of oval-shaped dilated rough endoplasmic reticulum (rER). Within the dilated rER, the mistlike deposit or deposit along the inner margin of the rER membrane was observed. On the other hand, BFA-treated cultured pituitary adenoma cells showed the opening of the cavity of the rER cisterna and they enlarged to an oval form with time and revealed an accumulation of electron-dense deposits within the dilated rER. These ultrastructural similarities between TSH cell adenoma and BFA-treated pituitary adenoma cells indicate the functional disturbances in the secretory passage through the Golgi apparatus in TSH cell adenoma cells.
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PMID:Ultrastructural characteristics of TSH-producing adenomas with special reference to its close similarity to BFA-treated pituitary adenoma cells. 1108 Dec 1

The oncogenes cyclin D1 and D3 are overexpressed in many tumors. Topoisomerase II alpha is found in proliferating cells. The immunohistological expression of cyclin D1, cyclin D3, and Topoisomerase II alpha was studied in a collection of 60 clinically inactive surgically removed pituitary adenomas of the follicle-stimulating hormone/luteinizing hormone (FSH/LH) cell complex (20 null cell adenomas, 20 oncocytomas, and 20 FSH/LH cell adenomas) for correlation with other proliferation markers (Ki-67, PCNA) and with clinical data. Whereas cyclin D1 was positive only in one invasive null cell adenoma (1.7%) with some p53-positive nuclei, cyclin D3 was overexpressed in the nuclei of 41 tumors (68%). Topoisomerase II alpha was demonstrated in the nuclei of 42 adenomas (70%) with no significant differences discernible between the three adenoma subtypes. There was no significant correlation to the time of development of tumor symptoms, but a correlation of Topoisomerase II alpha with cyclin D3 and the proliferation marker Ki-67 (Mib1). From these data we conclude that cyclin D3 and Topoisomerase II alpha appear to be additional markers for proliferation which can be used for prognosis index in surgical pathology of the pituitary.
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PMID:Cyclins D1 and D3 and topoisomerase II alpha in inactive pituitary adenomas. 1147 67

A 67-year-old woman presented with clinical features of hypercortisolism in association with an invasive pituitary macroadenoma. Adrenocorticotropic hormone (ACTH)-dependent Cushing's disease was documented, and the resected tumor was chromophobic, weakly positive with periodic-Schiff reagent, and showed immunostaining for ACTH and beta-endorphin in a minority of adenoma cells. Both luteinizing hormone and alpha-subunit staining were also observed, but no follicle-stimulating hormone reactivity was seen. Ultrastructurally, the tumor showed typical features of a gonadotroph adenoma of female type. Immunoelectron microscopy showed that ACTH was not produced in corticotrophs, but in cells with the characteristic features of gonadotrophs. This represents the second report of a plurihormonal gonadotroph adenoma producing sufficient ACTH to result in pituitary-dependent Cushing's disease.
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PMID:Cushing's disease due to plurihormonal adrenocorticotropic hormone and gonadotropin-producing pituitary adenoma. 1160 17


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