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At least 109 records · Page 6Linked to original sources
PubMed1964

SCINTILLATION SCANNING OF BRAIN TUMORS.

Brain scanning by means of externally placed moving scintillation detectors has proven to be an easy accurate method for demonstrating size, shape and position of many types of brain tumors. In a series of 53, there were few false negatives and few false positives. The procedure is easy on the patient, does not require anesthesia and can be done on outpatients. It is recommended as a screening procedure for all brain tumor suspects.

Astrocytoma↗
PubMed1998

Xanthomatous hypophysitis.

Inflammatory lesions of the hypophysis include lymphocytic hypophysitis, pituitary abscess, and granulomatous inflammation, with or without specific infections (i.e., sarcoidosis, mycobacteria). These lesions are known to mimic pituitary neoplasms. We report the clinical and pathologic findings in three patients who underwent transsphenoidal resection for presumed pituitary adenoma. Two were women aged 30 years (one with a 5-month history of headache, the other with a 1-year history of menstrual irregularity) and one was a 12-year-old girl with headache, nausea, and diabetes insipidus. Preoperative endocrinologic studies showed increased prolactin in one patient and normal serum thyroid stimulating hormone and prolactin levels in another. By magnetic resonance imaging (MRI), the first case had a 1.2-cm mass with increased signal on T1 and isointensity on T2, ring enhancement after gadolinium, and lateral deviation of the pituitary stalk. The second patient had a 1.1-cm "cystic" mass seen during magnetic resonance imaging with adjacent bony changes seen during computed tomography. In the third, computed tomography showed a hypodense pituitary mass that enlarged during 1-month observation. At surgery, abnormal soft tissue surrounded liquefied material in the anterior pituitary in all cases. Histologic studies showed fragments of intact normal anterior pituitary with preserved vascular and reticulin network and regions of anterior pituitary infiltrated by foamy histiocytes. Other fragments resembled granulation tissue, and some consisted of acellular debris. Histiocytes were immunoreactive for the macrophage marker CD68 and negative for S-100 and CD1a. Ultrastructurally, the normal adenohypophysis was permeated by lipid-laden macrophages. There were no well-formed granulomas or giant cells, hemosiderin, acid-fast bacilli, or fungi. Serial sections and keratin immunostains failed to identify an epithelial cyst lining or keratin among the debris. We propose the term "xanthomatous hypophysitis" for this lesion.

Adult↗
PubMed1979

A case of pituitary adrenocorticotropin-dependent Cushing's syndrome in the horse.

In the horse, a syndrome of hirsutism, hyperglycemia, glucosuria, polydipsia, polyuria, polyphagia, and progressive debilitation has been recognized. Most often the syndrome has been associated with adenomas of the pars intermedia of the pituitary and bilateral adrenal hyperplasia or nodular hyperplasia involving primarily the zona fasciculata. Previously, the syndrome has been ascribed to compression of the hypothalamus by an expanding but functionally inactive pituitary neoplasm. In the present case, with RIA determination of plasma ACTH concentrations, the syndrome was ascribed to pituitary ACTH-dependent hyperadrenocorticism and likened to human Cushing's disease.

Adrenocorticotropic Hormone↗
PubMed1984

Pituitary tumors.

The most frequent pituitary neoplasm is the adenoma, which can produce signs and symptoms owing to mass effects or secretion of pituitary hormones. The authors discuss these mass effects of pituitary tumors on the endocrine system and excess hormone secretion by pituitary adenomas.

Adenoma↗
PubMed1992

Morphologic effects of hGRH gene expression on the pituitary, liver, and pancreas of MT-hGRH transgenic mice. An in situ hybridization analysis.

Morphologic changes in the pituitary, liver, and pancreas of mice with the metallothionein-human growth hormone--releasing hormone (MT-hGRH) transgene were analyzed by in situ hybridization histochemistry (ISH). There was progression from somatotroph hyperplasia to neoplasia in pituitaries of transgenic mice. Pituitary neoplasms were present between 9 to 12 months of age in some mice. Magnetic resonance imaging (MRI) readily identified enlarged pituitaries in MT-hGRH transgenic mice. Serum mouse GH and hGRH levels were marked elevated in MT-hGRH transgenic mice. In situ hybridization histochemistry showed mRNA for hGRH in liver, pituitary, pancreas, spleen, and in most other tissues examined. Combined ISH and immunohistochemistry in the pituitary gland showed that some of the GH cells also produced hGRH, and ultrastructural immunohistochemical analysis of pituitaries showed that GH and hGRH were localized in the same cell and within the same secretory granules. Liver cells of MT-hGRH transgenic mice showed evidence of hypertrophy, and the pancreatic islets were hyperplastic with significant increases in the islet cell areas. The morphologic changes in the liver were distinctive enough to separate control littermates from MT-hGRH transgenic mice in all cases. The enlarged pancreatic islets had increased numbers of insulin-producing cells. Immunoreactive hGRH and hGRH mRNA were both localized in islet cells, and an intense hybridization signal of hGRH mRNA, but only weak staining for hGRH protein, were detected in the liver of transgenic mice. These results indicate that excessive hGRH production leads to distinct morphologic changes in various organs in MT-hGRH transgenic mice and that there is temporal progression from hyperplasia to adenomatous somatotrophs in pituitaries with chronic stimulation by hGRH that involves paracrine, endocrine, and autocrine mechanisms.

Adenoma↗
PubMed1999

Increased MEN1 mRNA expression in sporadic pituitary tumours.

BACKGROUND: The MEN1 gene on chromosome 11q13 encodes a tumour suppressor gene, mutations in which cause multiple endocrine neoplasia (MEN) type 1 syndrome. Loss of heterozygosity (LOH) at this locus is a common finding amongst sporadic pituitary tumours. We have therefore screened the MEN1 gene for mutations in sporadic pituitary tumours and, as the gene is a putative tumour suppressor, have quantified mRNA expression in tumorous and normal pituitaries to assess the role of MEN1 in pituitary tumorigenesis. SUBJECTS AND DESIGN: Thirty-one nonfunctioning pituitary tumours, 8 GH secreting, 2 TSH-secreting tumours and 1 corticotrophinoma have been assessed for the presence of MEN1 mutations, to examine the hypothesis that MEN1 mutations may contribute to the pathogenesis of sporadic pituitary neoplasms. In addition, quantitative changes in the pretranslational expression of the tumour suppressor gene MEN1 have been determined in 42 pituitary tumours and 6 normal pituitaries using semiquantitative reverse transcriptase PCR. RESULTS: No novel or previously published mutations were apparent in the MEN1 coding regions of any tumours studied, although several polymorphisms were identified. Transcriptional changes of the gene, assessed by semiquantitative RT-PCR, indicated that nonfunctioning and GH-secreting pituitary tumours are associated with significantly increased pretranslational expression of the MEN1 gene. In addition, the single corticotrophinoma showed increased expression compared to normal, as did one of the two TSH-omas. CONCLUSION: Coding mutations of the putative tumour suppressor gene MEN1 are unlikely to contribute to pituitary tumorigenesis in sporadic nonfunctioning, GH-secreting and TSH-secreting adenomas. Changes in pretranslational expression of MEN1 were observed in pituitary tumours, suggesting that changes in the level of MEN1 expression, rather than coding changes, may be of functional importance in influencing sporadic pituitary tumorigenesis.

Adenoma↗
PubMed1985

Immunocytochemistry of folliculo-stellate cells of normal and neoplastic human pituitary gland.

Five normal human pituitaries and 20 pituitary neoplasms were investigated by immunocytochemical methods. Glial fibrillary acidic protein and S100 have been shown in the anterior lobe of the pituitary. Both these markers were present in the folliculo-stellate cell. Evidence is presented for the presence of a transitional folliculo-stellate cell which is immunoreactive for S100. The role of the folliculo-stellate cell is discussed.

Glial Fibrillary Acidic Protein↗
PubMed1977

Chromosome banding patterns of two transplantable pituitary tumors induced in rats by 2,4,6-trimethylaniline.

The chromosomal constitution of a mammosomatotrophic and an inactive transplantable pituitary tumor induced in rats by 2,4,6-trimethylaniline was studied by the Giemsa-banding techniques. The inactive tumor line 7315i evolved from the active tumor line 7315a in one of the early transfers. A comparison was also made with chromosomal patterns of a transplantable rat hepatoma (7316A) induced by the same chemical carcinogen. Pituitary tumor line 7315a had a pseudotriploid complement with 63 chromosomes, whereas the inactive line 7315i was hypodiploid, with a dominant stemline of 36 chromosomes. The stemline chromosome number of the hepatoma was in the hypotetraploid region. Giemsa banding revealed that all chromosomes of the normal rat complement were present in both pituitary tumors. Four abnormal chromosomes were detected in the active tumor line and three in the inactive line. Both tumor lines contained a single minute chromosome. One common marker, a deleted chromosome No.1, was found in both pituitary tumors. This common marker chromosome was, however, not present in the hepatoma. The stemline karyotype of the hepatoma contained seven different markers, but none of them was identical to the abnormal chromosomes of the pituitary neoplasms. The findings suggested that the abnormal karyotypes of lines 7315a and 7315i could reflect the multisecretory activities of these neoplastic pituitary cells but that chromosomal localization of the secretory defect awaits exact genetic mapping of the rat chromosomes.

Aniline Compounds↗