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)

Prompted by a unique case of an ectomesenchymal chondromyxoid tumor (ECT) of the palate in a 54-year-old female, we reviewed the English and German literature on this entity until the end of 2016 using PubMed. The search produced 74 lingual cases with a nearly equal sex distribution and a mean age of 39.3 years, and two extra-lingual cases sharing histological and immunohistological features including nodular growth, round, fusiform or spindle-shaped cellular architecture, and chondromyxoid stroma. Immunophenotyping showed the majority of cases to be positive for glial fibrillary acidic protein (GFAP), S-100 protein, glycoprotein CD57, pancytokeratin (AE1/AE3), and smooth muscle actin (SMA); in isolated cases there was molecular-genetic rearrangement or gain of Ewing sarcoma breakpoint region 1 (EWSR1) but no rearrangement of pleomorphic adenoma gene 1 (PLAG1). At present, ectomesenchymal cells that migrate from the neural crest are considered to play a pivotal role in tumor origin. All cases had a benign course, although there were three recurrences. Because of the rarity of this tumor and the need for differential diagnostic differentiation from myoepithelioma and pleomorphic adenoma, both oral surgeons and pathologists should be aware of this entity.
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PMID:Ectomesenchymal chondromyxoid tumor: a comprehensive updated review of the literature and case report. 2949 57

The pathogenesis of Cushing's disease, which is caused by pituitary corticotroph adenoma, remains to be studied. Secreted angioinhibitory factor thrombospondin-1 (TSP-1) is an adhesive glycoprotein that mediates cell-to-cell and cell-to-matrix interactions and is associated with platelet aggregation, angiogenesis and tumorigenesis. We have found that the expression of TSP-1 is significantly lower in human pituitary corticotroph tumours compared with normal adenohypophysis. This study aims to elucidate the role of TSP-1 in regulating the tumour function of pituitary adenomas. Forced overexpression of TSP-1 in a murine AtT20 pituitary corticotroph tumour cell line decreased corticotroph precursor hormone proopiomelanocortin (POMC) transcription and adrenocorticotropic hormone (ACTH) secretion. Functional studies showed that TSP-1 overexpression in pituitary adenoma cells suppressed proliferation, migration and invasion. We have demonstrated that TSP-1 is a direct target of miR-449c. Further study showed that miR-449c activity enhanced tumorigenesis by directly inhibiting TSP-1 expression. Low expression of lncTHBS1, along with low expression of TSP-1, was associated with the high expression of miR-449c in Cushing's disease patients. Furthermore, RNA-immunoprecipitation associates miR-449c with lncTHBS1 suggesting that lncTHBS1 might be a negative regulator of miR-449c. Taken together, this study has demonstrated that lncTHBS1 might function as competing endogenous RNA for miR-449c, which could suppress the development of Cushing's disease.
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PMID:TSP-1 is downregulated and inversely correlates with miR-449c expression in Cushing's disease. 3101 50

The hormonal immunoreactivity and vascularity of pituitary adenomas containing folliculostellate (FS) cells have been compared with those of tumors in which such cells were not identified. FS cells were present in variable numbers in 36 of 92 tumors. Adenomas immunoreactive for growth hormone (GH), adrenocorticotropic hormone (ACTH), or prolactin (PRL) contained FS cells in 40-50% of cases. Those immunoreactive for glycoprotein hormones and alphasubunit contained FS cells in 67-85% of cases, a statistically significant correlation. When alpha-subunit was also present in GH-, GH/PRL-, and ACTH-immunoreactive tumors, a higher proportion contained FS cells (57-91%). These data suggest a correlation between the presence of FS cells and glycoprotein immunoreactivity in pituitary adenomas. Vascular channels identified by the binding of the lectinUlex europaeus were quantified in the two types of tumors. Those containing FS cells were not more vascular than those without FS cells, which suggests that FS cells do not play a significant role in the regulation of intratumoraf vascularization in human pituitary adenomas.
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PMID:Folliculostellate cells in pituitary adenomas: Studies of hormonal profile and tumor vascularity. 3235 34

The immunocytochemical profile of 300 clinically nonsecreting pituitary adenomas was investigated. All tumors were diagnosed, classified, and separated into null cell adenomas, oncocytomas, and gonadotroph adenomas according to their ultrastructural morphology. The immunocytochemical analysis was based on the semiquantitative proportional estimates of positive cells immunostained for all known peptide and glycoprotein pituitary hormones including alpha-subunit. The majority of tumors (87%) were to some extent immunopositive for various hormones. Glycoprotein hormones were most frequently encountered. Usually, particularly in males, more than one subunit was present in the same tumor. In 97 tumors (32%) more than 25% of adenoma cells were immunoreactive for gfycoprotein hormones. Fifty-five tumors (18%) contained occasional cells immunopositive for growth hormone (GH), prolactin (PRL), and adenocorticotropin (ACTH) in addition to glycoprotein hormones. Given the significant proportion of immunoreactive cells for gonadotropins and alpha-subunit, in tumors characterizedas null cell adenomas and oncocytomas, imrnunocytochemistry may provide valuable information to the pathologist and clinical endocrinologist contributing to the evaluation of this heterogeneous group of tumors.
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PMID:Null cell adenomas, oncocytomas, and gonadotroph adenomas of the human pituitary: An immunocytochemical and ultrastructural anafysis of 300 cases. 3237 Apr 37


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