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)

Human growth hormone (HGH) radio-immunoassay (RIA) was adapted for an accurate measurement of immunoreactive HGH concentrations in the CSF in different cases of hypothalamic-somatotropin dysfunctions. In control subjects (n = 43) mean HGH levels were 0.35 +/- 0.03 ng/ml in CSF and 1.95 +/- 0.2 ng/ml in plasma with a CSF/plasma ratio of 17%. The thyroid-stimulating hormone (TSH) RIA gave in controls mean basal levels of 2.65 +/- 0.2 muU/ml in CSF and 5.95 +/- 0.3 muU/ml in plasma with a CSF/plasma ratio of 44%. HGH and TSH concentrations in CSF and plasma show a very good correlation; but the regression curves for both hormones are distinctly different and appear specific for each polypeptide hormone. Hypothalamic-somatotropin hyperreactivity was reported in diabetic retinopathy (DR). CSF and plasma HGH concentrations in a group of diabetic patients with progressing retinopathy (n = 27) were not different from those in normal subjects (respectively 0.35 +/- 0.05 in CSF and 2.10 +/- 0.25 ng/ml in plasma with a CSF/plasma ratio of 16%). The HGH regression curve obtained in diabetics is similar to that of controls. These data do not substantiate the hypothesis of an HGH hyperreactivity in diabetic retinopathy. In somatotropin hypersecretion (acromegaly) without adenoma suprasellar extension, higher HGH concentrations recorded in CSF than in plasma cannot be attributed to an anatomical break-down of the CSF blood-brain barrier and suggest an active transport process of pituitary hormones to the CNS. HGH and TSH concentrations were measured in the cystic fluid of CNS tumors. In 1 case of a cystic dysembryoma, the HGH and TSH of CF were considerably increased. In gliomas (n = 8) the HGH and TSH cystic fluid concentrations were more elevated (respectively 0.72 +/- 0.2 ng/ml and 3.6 +/- 0.7 muU/ml) than in the CSF of controls.
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PMID:Distribution of growth hormone and thyroid-stimulating hormone in cerebrospinal fluid and pathological compartments of the central nervous system. 83 8

Radiosurgery (RS) is a new technique that is being developed worldwide to treat a variety of central nervous system (CNS) diseases. We report preliminary results concerning the first 35 patients treated at our institution between October 1989 and December 1990. These patients presented with pituitary adenomas (PA: 12 patients), primary CNS tumors with different histologies (11 patients), arteriovenous malformations (AVM: 6 patients), acoustic neurinomas (3 patients) and CNS metastases (3 patients). All patients were treated with a linear accelerator and received a single dose of 20 Gy delivered on the 70% isodose curve localized stereotactically by mean of either a CT scan or angiography. Preliminary results with a median follow-up of 26 months were as follows. AVM had totally disappeared in 3 patients after 12 and 17 months, and remained stable in 3 at 6 and 26 months. In 3 PA patients, the adenoma was partially regressed on the CT scan and, in 2 patients, the visual field was moderately improved; none experienced clinical improvement due to hormonal hypersecretion. One patient with neurinoma experienced clinical improvement, but the CT scan remained unchanged in the 3 patients. Of the patients with primary or secondary tumors, 8 exhibited a reduced lesion diameter on the CT scan, but 3 died later of progressive disease. Complications were not rare. In 7 patients, delayed reactions were observed: one case of cerebral edema reversed under corticotherapy; and 6 cases of neurological impairment due to brain necrosis, reversed in only one. RS appears to be an interesting approach for the treatment of deeply located AVM and for small acoustic neurinomas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Stereotactic radiosurgery. Preliminary experience of a team of Lyon]. 850 25

Neurothelin/HT7, a transmembrane glycoprotein of the immunoglobulin superfamily, is a marker of blood-brain barrier (BBB)-forming endothelial cells. We have studied the expression of neurothelin in tumors grown on the chorioallantoic membrane (CAM) of chick embryos. We inoculated each 3-5 x 10(6) rat C6 glioma, rat 10AS pancreatic carcinoma, human A375 melanoma, and human mammary duct adenoma cells on the CAM of 10-day-old chick embryos. The tumors were harvested on day 17. All four tumor cell lines formed solid tumors which were supplied by vessels of CAM origin. Foci of bleeding were regularly observed within the tumors. All four tumors induced the expression of neurothelin/HT7 (but not of glucose transporter-1) in tumor endothelial cells, whereas expression in adjacent endothelial cells of normal CAM did not occur. Confocal laser scanning microscopy revealed that the pattern of neurothelin expression in tumor endothelial cells was different from that in normal central nervous system (CNS) endothelium, but the relative molecular weight of neurothelin, studied by western blot analysis, was the same in brain and in tumors. It has been shown that, with increasing malignancy, vessels of CNS tumors lose their morphological characteristics, and BBB markers such as the glucose transporter-1 are downregulated. Our results show that, in contrast, the BBB marker, neurothelin, is expressed de novo in tumor endothelial cells. Potential common functions of neurothelin in endothelial cells of the CNS and tumors are discussed.
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PMID:Induction of the blood-brain barrier marker neurothelin/HT7 in endothelial cells by a variety of tumors in chick embryos. 1076 63

Hyperparathyroidism onset at a young age is one feature in multiple endocrine neoplasia (MEN) type 1 and MEN type 2A cancer syndromes. There are several case reports of MEN Type 1-associated central nervous system (CNS) tumors. To determine if there is an association between parathyroid adenomas and CNS tumors, we used Swedish registry data to identify all individuals operated on for parathyroid adenomas between 1958-99 (n = 12,468). Follow-up for the occurrence of CNS tumors in these individuals was through linkage with the Swedish Cancer Registry. There were 70 observed cases of a CNS tumor diagnosed after a parathyroid adenoma, to be compared to 35 expected (standard incidence ratio [SIR] = 2.0; 95% confidence interval [CI] = 1.5-2.5). This increased risk was independent of duration of follow-up and was confined to meningiomas (SIR = 2.4, 95% CI = 1.7-3.4) and neurinomas (SIR = 3.4, 95% CI = 1.5-6.8). These results strongly indicate an association between these tumor forms that may be genetic, environmental (such as radiation) or a combination of both.
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PMID:Parathyroid adenoma and primary CNS tumors. 1551 18

Ectopic adrenal cortical neoplasms are extremely rare; few involve the central nervous system (CNS). We report a 17-month-old girl with spinal adrenal cortical neoplasms. She was unable to crawl or stand and was irritable at night. Her appearance was asymmetrical; the right side of her face and her lower right leg were enlarged. In addition, she manifested hyperplasia of the thymus, fibrous hyperplasia of the bladder, and hamartoma in the liver. However, all abnormalities were asymptomatic. Magnetic resonance imaging (MRI) revealed well-circumscribed masses within the dura mater at the T12-L1 and L3-L4 level. Histology disclosed that the lesions were composed of sheets and nests of round and polygonal cells with mostly round regular nuclei; eosinophilic to clear cytoplasm was abundant. Immunohistochemically, the tumor cells were strongly positive for inhibin-alpha, positive for synaptophysin and vimentin, and negative for GFAP, EMA, S-100, NSA, and chromogranin A. In addition, the nuclei stained positive for steroidogenic factor 1 (Ad4BP/SF-1), which is involved in adrenal steroidogenesis. This case confirms the occurrence of adrenocortical adenoma in the CNS. We suggest that this tumor should be considered in the differential diagnosis of CNS tumors.
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PMID:Ectopic adrenal cortical adenoma in the spinal region: case report and review of the literature. 2104 15

Classified as benign central nervous system (CNS) tumors, pituitary adenomas account for 10% of diagnosed intracranial neoplasms. Although surgery is often curative, patients with invasive macroadenomas continue to experience significant morbidity and are prone to tumor recurrence. Given the identification of human brain tumor-initiating cells (TICs) that initiate and maintain tumor growth while promoting disease progression and relapse in multiple CNS tumors, we investigated whether TICs also drive the growth of human pituitary adenomas. Using a nanoString-based 80-gene custom codeset specific for developmental pathways, we identified a differential stem cell gene expression profile within human pituitary adenomas. Prospective functional characterization of stem cell properties in patient-derived adenomas representing all hormonal subtypes yielded a subtype-dependent self-renewal profile, which was enriched within the CD15+ cell fraction. The tumor-initiating capacity of CD15high adenoma cells was assayed in comparison to CD15low adenomas using in vivo limiting dilutions, which maintained the rare frequency of TICs. Repeated analyses using sorted cell populations for CD15+ TICs compared to CD15- adenoma cells provided further evidence of xenograft tumor formation to support CD15+ cells as putative pituitary adenoma-initiating cells (PAICs). The clinical utility of our findings was established through in silico analyses and comparative gene expression profiling of primary and recurrent pituitary adenomas. CD15 was enriched in recurrent adenomas, which was validated using routine clinical immunohistochemistry in a limited number of samples. Our work reports the first prospective identification of human PAICs using CD15. Patients with CD15high adenomas may therefore benefit from more aggressive surgical interventions and chemo/radiotherapy.
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PMID:The identification of human pituitary adenoma-initiating cells. 2789 39

The 4th edition of the World Health Organization (WHO) classification of endocrine tumors has been recently released. In this new edition, major changes are recommended in several areas of the classification of tumors of the anterior pituitary gland (adenophypophysis). The scope of the present manuscript is to summarize these recommended changes, emphasizing a few significant topics. These changes include the following: (1) a novel approach for classifying pituitary neuroendocrine tumors according to pituitary adenohypophyseal cell lineages; (2) changes to the histological grading of pituitary neuroendocrine tumors with the elimination of the term "atypical adenoma;" and (3) introduction of new entities like the pituitary blastoma and re-definition of old entities like the null-cell adenoma. This new classification is very practical and mostly based on immunohistochemistry for pituitary hormones, pituitary-specific transcription factors, and other immunohistochemical markers commonly used in pathology practice, not requiring routine ultrastructural analysis of the tumors. Evaluation of tumor proliferation potential, by mitotic count and Ki-67 labeling index, and tumor invasion is strongly recommended on individual case basis to identify clinically aggressive adenomas. In addition, the classification offers the treating clinical team information on tumor prognosis by identifying specific variants of adenomas associated with an elevated risk for recurrence. Changes in the classification of non-neuroendocrine tumors are also proposed, in particular those tumors arising in the posterior pituitary including pituicytoma, granular cell tumor of the posterior pituitary, and spindle cell oncocytoma. These changes endorse those previously published in the 2016 WHO classification of CNS tumors. Other tumors arising in the sellar region are also reviewed in detail including craniopharyngiomas, mesenchymal and stromal tumors, germ cell tumors, and hematopoietic tumors. It is hoped that the 2017 WHO classification of pituitary tumors will establish more biologically and clinically uniform groups of tumors, make it possible for practicing pathologists to better diagnose these tumors, and contribute to our understanding of clinical outcomes for patients harboring pituitary tumors.
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PMID:The 2017 World Health Organization classification of tumors of the pituitary gland: a summary. 2882 44

The simultaneous development of two or more primary central nervous system (CNS) tumors of different cell types represents 0.9% of all diagnosed CNS tumors. To the best of our knowledge, the simultaneous occurrence of glioblastoma and pituitary adenomas has been reported four times in the English literature, with only two cases harboring prolactinoma and glioblastoma. We report a case of a 42-year-old male who was diagnosed with a sporadic co-occurrence of glioblastoma and a prolactin-secreting pituitary adenoma (prolactinoma). This case report discusses the clinical presentation, radiological/histopathological features, and outcome as well as reviewing the pertinent medical literature. Glioblastoma and a prolactin-secreting adenoma may be detected within the same patient. Further studies are required to delineate the tumorigenesis of the development and co-occurrence of multiple intracranial tumors.
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PMID:Glioblastoma and prolactinoma: a rare simultaneous occurrence. 3078 3