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

During the period 1950-81, 678 cases of primary hyperparathyroidism were surgically treated at University College Hospital, London. The causes were a single adenoma in 575, two adenomas in 25, carcinoma in 20 (two of which had coexistent adenomas), chief cell hyperplasia in 56, and water clear cell hyperplasia in two. Histological diagnosis is not difficult except in some cases of carcinoma and in a few in which differentiation between recurrent hyperplasia and recurrent carcinoma is exceptionally difficult. In this paper we review all the cases of primary carcinoma of the parathyroid seen during this period to define those pathological features of value in the diagnosis.
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PMID:Histological diagnosis of carcinoma of the parathyroid gland. 651 82

The molecular basis for parathyroid carcinoma remains undetermined. Parathyroid carcinoma potentially remains curable by early en bloc resection. This requires a reliable diagnostic tool as histological features alone are insufficient to distinguish parathyroid carcinoma from its benign counterpart, parathyroid adenoma. A variety of human cancers arise from the inactivation of the retinoblastoma (RB) gene, a tumour-suppressor gene on chromosome 13q14. We investigated the role of this gene in parathyroid growths by using a mouse monoclonal antibody to detect RB gene expression immunohistochemically. Two of the three parathyroid carcinomas in this study showed evidence of RB gene inactivation compared with one of 11 benign parathyroid entities. Three normal parathyroid glands stained showed strong evidence of RB gene expression in all three glands. The relationship between RB gene inactivation and parathyroid malignancy, however, was not statistically significant.
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PMID:Inactivation of retinoblastoma gene in malignant parathyroid growths: a candidate genetic trigger? 748 9

Studies have demonstrated the presence of epidermal growth factor receptors in human parathyroid tumors. However, there is little information on the effect of other peptide growth factors on parathyroid cell growth. We therefore studied the interaction of insulin-like growth factor I (IGF-I) with human parathyroid tumor cells. Parathyroid tissues were obtained from 24 patients with primary or secondary hyperparathyroidism. There were 15 solitary adenomas, 5 carcinomas, and 4 hyperplastic tissues. First, the binding of [125I]IGF-I to the crude membrane fractions was studied by competitive inhibition with unlabeled IGF-I. Second, isolated parathyroid cells were cultured with IGF-I and examined for DNA synthesis. The IGF-binding protein (IGFBP) content of tissue homogenates was determined by ligand blot analysis. The binding of [125I]IGF-I to parathyroid membranes was dependent on time, temperature, and pH of the medium. Maximum binding was obtained after incubation for 18 hours at 4 degrees C. Specific binding to parathyroid cancer membranes (mean +/- SE, 10.75 +/- 10.55%/mg protein) was significantly (p < 0.05) greater than that in adenoma tissues (3.71 +/- 2.11%/mg). The value in hyperplastic tissues (4.78 +/- 2.97%/mg) was not different from that in adenomas. Affinity cross-linking and autoradiography demonstrated the type I IGF receptors. Cultured parathyroid cells responded to IGF-I with increased DNA synthesis. The parathyroid tumor tissues expressed IGFBPs. These results suggest that IGF-I and IGFBPs are involved in the growth regulation of parathyroid tumor cells.
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PMID:Insulin-like growth factor I receptors and insulin-like growth factor-binding proteins in human parathyroid tumors. 753 95

Primary hyperparathyroidism is a chronic, multi-system disease due to an overproduction of PTH from adenoma, hyperplasia or carcinoma of the parathyroid. Classical disease type classification consisted of bone type, kidney type and latent or chemical type. Though a longer course is usually associated with more severe involvement of especially the skeletal system and larger tumor size, the progression of the disease is not always uniform. Rapid tumor growth may be associated with shorter course and more extensive involvement. The role of PRAD1, a DNA sequence near the PTH gene on chromosome 11 possibly related to tumor growth, should further be investigated with reference to the disease types and courses of the disease.
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PMID:[Primary hyperparathyroidism. Concept, classification and symptomatology]. 775 72

Parathyroid carcinoma is a rare cause of hyperparathyroidism. Histological differentiation from parathyroid adenoma may be difficult and is rarely achieved intraoperatively. Parathyroid carcinomas are sometimes localized heterotopically. We report a case of parathyroid cancer in the left thyroid lobe. Surgical therapy should include en bloc resection of the tumor, the thyroid lobe and the parathyroid tissue.
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PMID:[Primary hyperparathyroidism in intrathyroid parathyroid cancer]. 830 61

The distribution and expression of parathyroid hormone (PTH) were investigated in normal and abnormal parathyroid tissue. PTH was detected using a monoclonal antibody with specificity for the 44-68 region of the PTH molecule. Prominent reactivity for PTH was seen in normal parathyroid with a granular pattern of staining. Active parathyroid tissue (adenoma and hyperplasia) showed much less reactivity for PTH, although there was prominent reactivity in the normal tissue around adenomas. Comparison of expression of PTH with that of parathormone mRNA showed a reciprocal pattern in normal tissue and, to a less marked extent, in abnormal tissue. Parathyroid carcinoma in particular had coinciding areas of PTH and PTH mRNA expression. Oxyphil cells had little or no PTH expression, except in the associated 'colloid' in some cases. The findings indicate an inverse relationship between storage and cellular synthesis of PTH, this being more marked in physiological than in pathological conditions of the parathyroid.
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PMID:In situ correlation of synthesis and storage of parathormone in parathyroid gland disease. 843 15

The epidermal growth factor receptor (EGFr) family has been increasingly recognized as an important component in the control of normal cell proliferation and the pathogenesis of cancer. We have studied EGFr expression in 104 cases of hyperparathyroidism by immunocytochemistry (ICC) and by in situ hybridization (ISH). Using two different monoclonal antibodies, ICC for EGFr was performed on 66 cryostat sections and 38 wax-embedded parathyroid glands. ISH was performed on 49 of these glands using a cocktail of three anti-sense probes to EGFr mRNA and a nonspecific control probe to human HPV-18 virus. Breast and prostate tumors were employed as positive controls for both ICC and ISH. Controls demonstrated positive EGFr staining. None of the 104 parathyroid glands showed any ICC positivity. ISH displayed positive staining for EGFr mRNA in five of six carcinomas and eight of nine nonrenal hyperplastic glands. Only 3 of 15 adenomas and 3 of 19 renal hyperplastic glands showed positive staining. This difference was statistically significant between adenoma and carcinoma (p < 0.05) and between adenoma and nonrenal hyperplasia (p < 0.01) (Tukey's multiple comparison test). This study demonstrates that EGFr mRNA is present in parathyroid tumors. Expression in carcinoma and nonrenal hyperplasia is significantly different from adenoma and renal hyperplastic glands. In contrast, ICC failed to demonstrate EGFr protein expression. These findings suggest that either receptor numbers are too low to detect by ICC or there is a failure of mRNA translation. More studies are needed to establish whether the EGFr plays a role in the development of parathyroid cancer or hyperplasia.
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PMID:Epidermal growth factor receptor status in hyperparathyroidism: immunocytochemical and In situ hybridization study. 867 44

Neck exploration due to suspicion of primary hyperparathyroidism (pHPT) was performed in 309 instances (298 patients) during a 17 year period, in 44 instances (14%) as a second operation after former goitre surgery or surgery for pHPT. Adenomas were found in 247 patients (83%), 12 patients had double adenomas and one triple adenoma. Hyperplasia was registered in 34 patients (11%) and three had parathyroid cancer. Median weight of adenomas was 1200 mg and hyperplasia 1500 mg. In 14 patients only normal glands were identified. In six of these 14 patients the diagnosis was later withdrawn. In 276 out of 292 patients with pHPT normocalcaemia was established, 16 patients remained hypercalcaemic. Success-rate concerning verification of pHPT was therefore 97% (284 out of 292) and concerning attainment of normocalcaemia 95% (276 out of 292). There was one perioperative death due to myocardial infarction. Four patients had transient unilateral recurrent nerve injury. In one patient with parathyroid cancer vocal cord paralysis was permanent. Follow-up after at least one year revealed normocalcaemia in 91% of the patients, hypercalcaemia in 7% and hypocalcaemia in 2%. Twenty percent of the patients had died 0-12 years, median 2.8 years postoperatively. Death was related to the degree of hyperparathyroidism evaluated by weight of abnormal parathyroid tissue.
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PMID:[Surgical treatment of primary hyperparathyroidism]. 992 95

Most cases of primary hyperparathyroidism are due to either a parathyroid adenoma or to parathyroid hyperplasia. Parathyroid carcinoma is a very rare cause of hyperparathyroidism. Although the diagnosis of parathyroid carcinoma is usually established based on pathological criteria of vascular and capsular invasion, some clinical and biochemical features differentiate it from benign forms of hyperparathyroidism. We report the case of a middle-aged woman with a long standing history of nephrolithiasis, who presented with a palpable neck mass, weight loss, severe hypercalcemia and hypophosphatemia, as well as very high serum levels of intact parathyroid hormone. Surgical neck exploration revealed a large tumor that invaded trachea, esophagus, reccurrent laryngeal nerve, right apical pleura and right carotid artery. Pathological examination confirmed the invasive nature of the tumor. Along with the case report, we review the literature and discuss the diagnostic and therapeutic options of this rare condition.
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PMID:Primary hyperparathyroidism due to parathyroid carcinoma. 920 27

Primary hyperparathyroidism is characterized by hypercalcemia and elevated parathyroid hormone levels. It can be caused by overactivity of one (adenoma or carcinoma) or more (hyperplasia or multiple adenoma) parathyroid glands. Parathyroid adenoma and hyperplasia are usually mono- or oligoclonal neoplasms. To establish whether parathyroid cancer has a genetic composition distinct from parathyroid adenoma, we analyzed 10 adenoma and 10 carcinoma cases by comparative genomic hybridization (CGH). Results show clear differences between the constitution of adenoma and carcinoma genomic DNA. The most frequent genomic alterations in adenoma included deletions on chromosomes 11, 17 (5 of 10 cases), and 22 (7 of 10 cases). In parathyroid carcinoma, frequent chromosomal deletions were on chromosome arm 1p (4 of 10 cases) and chromosome 17 (3 of 10 cases), and gains were on chromosome 5 (3 of 10 cases). Our data indicate that different genetic changes could contribute to the development of parathyroid adenoma and carcinoma; genomic losses predominate in adenoma, and gains along with some losses are found in carcinoma. Furthermore, the CGH results implicate several chromosomal regions that may harbor genes that could be potentially involved in the development of parathyroid adenoma and carcinoma.
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PMID:Comparative genomic hybridization analysis of human parathyroid tumors. 977 6


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