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)

We have investigated the possibility that local production of GHRH within the adenohypophysis could be an aetiological factor in the development of human pituitary somatotroph and other tumours. We examined 51 human pituitary adenomas for GHRH transcripts using in situ hybridization histochemistry. GHRH transcripts were identified in 13 of 17 somatotroph adenomas, 4 of 10 corticotrophs, 1 of 6 lactotrophs and 1 of 18 endocrinologically inactive adenomas. In 11 GHRH-expressing somatotroph adenomas, SRIH transcripts were also identified. In all cases except one (a corticotroph adenoma) the average number of GHRH transcripts exceeded that found in the arcuate nucleus of simultaneously hybridized rat brain sections. In some pituitary adenomas, GHRH transcripts were clearly localized to a discrete subpopulation of cells and in these, the amount of GHRH mRNA per cell was comparable to that found in the GHRH-expressing cells of the rat arcuate nucleus. Although we have not directly demonstrated an association between the two, the identification of localized, high level GHRH gene expression in somatotroph adenomas suggests that GHRH may have a role in pituitary adenoma formation.
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PMID:Growth hormone-releasing hormone transcripts in human pituitary adenomas. 135 May 90

The DNA from a pituitary adenoma of a patient with multiple endocrine neoplasia (MEN) type 1 was analyzed to detect a point mutation of the Gs alpha gene (gsp) by the PCR direct-sequencing method. The patient had galactorrhea, amenorrhea and acromegalic features. Hormonal examination revealed high serum levels of PRL and GH. The tumor was histologically diagnosed as a mixed GH cell-PRL cell adenoma in which GH and PRL were produced by different cells. Sequence analysis of the DNAs extracted from paraffin sections of pituitary, parathyroid, and pancreas tumors demonstrated the substitution of thymidine for cytidine in codon 201 of the Gs alpha gene that resulted in replacement of arginine (CGT) with cysteine (TGT) only in the pituitary adenoma, but not in the parathyroid and pancreas tumors. These results suggest that a pituitary specific point mutational activation of the Gs alpha gene may be involved in the development of the pituitary adenoma in this patient.
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PMID:A pituitary specific point mutation of codon 201 of the Gs alpha gene in a pituitary adenoma of a patient with multiple endocrine neoplasia (MEN) type 1. 135 1

We report a case of pituitary adenoma in association with parathyroid carcinoma as an unusual combination of multiple endocrine neoplasia (MEN). A 48-year-old man had a trans-sphenoidal hypophysectomy and transcranial partial removal of a recurrent pituitary chromophobe adenoma followed by a course of radiotherapy in 1980. Four years later, he developed hypercalcemic crisis from a parathyroid carcinoma with invasion to the adjacent thyroid gland and skeletal muscle. A hemithyroidectomy and resection of the left lower parathyroid gland was performed. Three years later, he had local recurrence and anterior chest wall metastasis accompanied by hypercalcemia. After resection of the remnant and metastatic lesion, eucalcemia was achieved. There was no family history of endocrine tumors. This case illustrates the rare association of a malignant parathyroid tumor and a chromophobe adenoma of the pituitary as a variant of MEN syndrome.
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PMID:Parathyroid carcinoma in a patient with non-secretory pituitary tumor: a variant of multiple endocrine neoplasia type-I? 135 78

In addition to the common presentations of the multiple endocrine neoplasia (MEN) syndromes, unusual organ involvement as rare manifestations of a single disease may occur. Among our patients we have identified four cases in which unusual features of MEN were present. In the first patient, bilateral adrenal cortical adenoma, parathyroid adenoma, multiple pancreatic tumors, and follicular thyroid carcinoma were observed. The second patient suffered from thymic carcinoid, parathyroid hyperplasia, gastrinoma, and pituitary adenoma. Additionally, one family was discovered in which medullary thyroid carcinoma (MTC), Hirschsprung's disease, and pheochromocytoma occurred and another family had MTC and ovarian cancer. Based on these observations, we stress the importance of screening for MEN syndromes in all patients with pathologic findings in any endocrine organ.
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PMID:Unusual features of multiple endocrine neoplasia. 136 16

Various functioning and non-functioning tumors arise from endocrine glands in both the sporadic and familial forms and pathophysiology of the tumors is variable due to differences in the sort of tumor-bearing endocrine organs and in the amount of hormones released. In this paper, gene abnormalities in growth hormone (GH)-secreting pituitary adenoma, ectopic GHRH-producing tumor, multiple endocrine neoplasia (MEN) and ectopic parathyroid hormone (PTH)-producing tumor are documented in relation to etiology and pathophysiology. GH-secreting pituitary adenoma is heterogeneous in clinical features, pathological findings and GH responses to various secretagogues. A point mutation of codon 201 of Gs alpha gene was observed in 2 out of 45 GH-secreting pituitary adenomas (4.4%), but no point mutation of Gi2 alpha gene was found. Pituitary tumors may occur at any stage of differentiation from the totipotent cells to mature anterior pituitary cells, and the mutations of Gs alpha and H-ras genes as well as loss of heterozygosity (LOH) found on chromosome 11 in some adenomas must be involved in their tumorigeneses. Since 1959, 34 patients with ectopic GHRH-producing tumor associated with acromegaly have been reported. In our case of MEN type 1, the paradoxical rise of plasma GH after TRH or glucose administration disappeared after resection of the tumor. The tumor cells showed neither rearrangement nor amplification of GHRH gene and 20 oncogenes including ras, myc, and erb. Only LOHs of HRAS1 and D11S151 were detected in this tumor, but no point mutation was found in HRAS1 gene. Therefore, a kind of tumor suppressor gene may be involved in the tumorigenesis of the tumor in addition to inactivation of MEN-1 locus. In MEN-1 patients, we reported LOH on chromosomes 1, 9, 11 and 16, while we reported point mutation as being present only in Gs alpha gene on chromosome 20. This point mutation was found specifically in GH-secreting pituitary adenoma but not in hyperplastic parathyroid and pancreas adenoma. These data suggest that in MEN-1 patients tumorigenesis occurs and advances from hyperplasia and adenoma to cancer during multistep changes of genes such as inactivation of MEN-1 gene and other tumor suppressor genes and activation of oncogenes. Ectopic PTH-producing tumor was first reported by us in 1989, and this was followed by 2 papers. These patients showed a disturbance of consciousness and high levels of serum calcium and plasma PTH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathophysiology and gene abnormalities of endocrine tumors]. 136 16

In 48 patients undergoing transsphenoidal surgery for pituitary adenoma, the intrasellar pressure was recorded during surgery. In 14 patients, adenoma blood flow was measured with the technique of local injection of 133xenon. Median intrasellar pressure was 30 mmHg (range 8-62), n = 48, and median adenoma blood flow was 8 ml/100 g/min (range 0-37), n = 14. In two patients, blood flow in the anterior pituitary gland was measured, and values of 26 and 22 ml/100 g/min were obtained. The finding that intrasellar pressure is above central venous and intracranial pressure suggests the possibility that the adenoma and the anterior pituitary gland are supplied not only with venous blood, but receive an additional arterial supply at a less than normal arterial pressure. In three cases perfusion pressures that caused arrest of adenoma blood flow were found, and these observations are discussed with reference to pituitary apoplexy.
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PMID:Pressure and blood flow in pituitary adenomas measured during transsphenoidal surgery. 138 27

We have studied seven patients with a clinically nonfunctioning or alpha-subunit-secreting pituitary macroadenoma, four of whom received long term, high dose octreotide treatment. We have attempted to correlate the presence of somatostatin receptors (SS-R) in the adenomas and the outcome of octreotide treatment, as measured by tumor size, improvements in visual field defects, and hormonal response. The presence of SS-R in the pituitary adenomas was demonstrated in vivo using [111indium]octreotide scintigraphy and in vitro by autoradiography of tissue fragments obtained after transsphenoidal surgery. Adenomas from six of the seven subjects were SS-R positive. High dose (1200 micrograms, sc, daily) octreotide treatment was given to four subjects, three of whom were SS-R positive. Improvement of the visual field defects was observed in three of four patients (including the SS-R-negative subject), although no computed tomographic scan-assessed tumor size reduction was found. Two of four patients showed small but significant reductions in serum FSH concentrations (to 83% and 93% of initial values) with treatment. These in vivo responses to high dose octreotide treatment could not be predicted by pretreatment responses to 200 micrograms TRH or 100 micrograms octreotide. Tissue fragments for cell culture were obtained from six patients, and in vitro release of gonadotropins and/or alpha-subunit could be demonstrated in five cultures. In vitro, octreotide (10 nmol/L) significantly decreased gonadotropiin or subunit release in three of five cultures, whereas bromocriptine (10 nmol/L) significantly reduced the release in four of five cultures and to a significantly greater extent than octreotide. In conclusion, in six of seven patients with a clinically nonfunctioning or alpha-subunit-secreting pituitary adenoma, SS-R were demonstrated in the tumor. In vitro incubation of adenoma cells with octreotide resulted in mild inhibition of gonadotropin or alpha-subunit release. Although in vivo long term treatment with high doses of octreotide did not result in substantial tumor size reduction, improvement of visual field defects was observed in three of four subjects.
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PMID:Clinically nonfunctioning pituitary adenoma and octreotide response to long term high dose treatment, and studies in vitro. 143 93

A multivariant analysis was carried out in 120 patients with pituitary adenoma (prolactinoma, HGH-secreting adenoma and nonfunctional adenoma) and an equation was obtained concerning the prolactinoma (whose independent variables were age, galactorrhea, impotence, stage, and pretreatment secretion of ACTH) and another one concerning the nonfunctional adenoma (with age evolution time, visual disturbance evolution and galactorrhea as independent variables). These equations are useful in the differential diagnosis. The internal validity of both equations was obtained by calculating the ROC curve and determining sensibility, specificity and predictive values at the "optimum point" of this curve.
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PMID:A multivariant study of pituitary adenoma, obtainment of two logistic regression equations as an auxiliary support in the diagnosis of these tumors. 143 39

We report a 44-year-old male with a thyrotropin (TSH)-secreting pituitary adenoma. Based serum free triiodothyronine (FT3, 12.1 pmol/l) and free thyroxine (FT4, 28 pmol/l) were increased with normal basal TSH (3.1 mU/l). There was impaired TSH response to thyrotropin releasing hormone (TRH) test. Serum TSH was suppressed to 59% of the basal level after oral administration of 1.4 mg 3,3'-5-triiodothyroacetic acid (triac), whereas no suppression was observed after 75 micrograms daily administration of triiodothyronine (T3). Serum concentrations of alpha-subunit of TSH (TSH-alpha) and TSH-alpha/TSH molar ratio were high, being 1.95 micrograms/l, and 4.4, respectively. Pituitary CT and MRI scan showed the presence of a macroadenoma in the anterior lobe of the pituitary gland. Histopathology of the excised pituitary confirmed the diagnosis of a TSH-producing adenoma. A positive correlation between TSH and FT3 (r = 0.66, P less than 0.01) or FT4 (r = 0.54, P less than 0.01) was observed in serial sera obtained before and after operation.
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PMID:Thyrotropin-secreting pituitary adenoma: a case report. 144 57

We studied 40 endocrinologically inactive pituitary adenomas by immunohistochemistry, electron microscopy, and cell culture in order to determine the incidence of gonadotropic adenomas and to classify nonfunctioning adenomas. Immunohistochemical studies using a large panel of monoclonal and polyclonal antibodies identified the following nonfunctioning adenomas: 20 gonadotropic adenomas, four silent corticotropic adenomas, one plurihormonal adenoma, and 15 nonsecreting adenomas. Among nonsecreting adenomas, ultrastructural study of 13 cases identified seven null cell adenomas and six oncocytomas. Silent corticotropic adenomas were classified into subtypes I, II, and III according to Kovacs and Horvath. Most often, gonadotropic adenomas displayed a varying number of oncocytic cells, characteristic secretory granules, and a prominent Golgi apparatus. Postembedding immunoelectron microscopy was performed on eight gonadotropic or nonsecreting adenomas, but this technique did not provide any additional information. Six gonadotropic adenomas and 10 so-called nonsecreting adenomas were studied in primary cell cultures. The six gonadotropic adenomas and seven of the 10 nonsecreting adenomas released gonadotropins in the culture medium. The use of in vitro results as a supplementary diagnostic criterion allowed classification of the 40 nonfunctioning adenomas as follows: 27 gonadotropic adenomas, four silent corticotropic adenomas, one plurihormonal adenoma, and eight nonsecreting adenomas. These results demonstrate a high proportion of gonadotropic adenomas among nonfunctioning adenomas (67.5%) and the usefulness of several techniques in characterizing this type of pituitary adenoma.
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PMID:Contribution of immunohistochemistry, electron microscopy, and cell culture to the characterization of nonfunctioning pituitary adenomas: a study of 40 cases. 146 69


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