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Results for “parathyroid carcinoma”

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PubMed1994

[Isolated thyroid and skin metastases of renal carcinoma].

Metastases to the thyroid gland from renal carcinoma are observed in 10% of the uncommon metastatic thyroid tumours. They are the first sign of renal carcinoma in 25% of cases or appear after primary treatment of renal neoplasia, up to 27 years later. Metastases are more frequent in pathological glands, perhaps because intraparenchymal blood flow is slowed and tissue oxygen partial pressure is reduced. Thyroid metastases are frequently associated with lung ones, whether those associated with metastases to other organs (duodenum, pancreas, skin) are very unusual. Clinical manifestations are thyroid node without hormonal modifications or acute swelling of the gland with hormonal hyperfunction; other signs are dysphonia and/or dysphagia. Thyroid nodes are "cold" at 131I scanning and with mixed structure at ultrasonography. Fine needle aspiration is often diagnostic. Problems in differential diagnosis are among clear-cell renal carcinoma and some types of thyroid adenoma, adrenal carcinoma, parathyroid carcinoma, testicular seminoma and hypernephroid thyroid carcinoma. Treatment is surgical: subtotal or total lobectomy, with or without isthmectomy, if metastasis is single, total thyroidectomy in diffuse disease. Some Authors always choice total thyroidectomy to erase microscopic foci of disease in contralateral lobe. Reported survival after treatment is from a few months to 27 years. Survival is longer with a metastasis appearing after nephrectomy and with unique versus multiple ones.

Abdominal Muscles↗

PubMed1981

Carcinoma of the parathyroid gland. A light and electronmicroscopic study.

The morphological features of a functional parathyroid carcinoma in a 34-year-old female are presented. The case was unique in the high frequency of mitotic figures permitting a tentative diagnosis of malignancy already on frozen sections. The parathyroid nature of the lesion was established ultrastructurally by demonstration of secretory granules, glycogen particles and lipid material within the cytoplasm. Also noteworthy was the presence of annulate lamellae, denoting rapidly growing tissue. Few examples of this lesion are at hand, and ultrastructural studies which provide valuable information regarding the site of origin, have previously been recorded in only 6 publications.

Adult↗

PubMedDate not supplied

[Cervico-mediastinal carcinoma of the parathyroid: report of a case].

Parathyroid carcinoma is a rare malignancy. We report the case of a 66 years old man referred to our department for a large substernal goiter suspected as a thyroid cancer associated with severe hyperparathyroidism. After normalization of serum levels of calcemia, total thyroidectomy and subtotal parathyroidectomy was performed. Histopathology revealed a parathyroid cancer of 450 g.

Adenocarcinoma, Clear Cell↗

PubMed1980

[Hyperparathyroidism in carcinoma of the parathyroids (author's transl)].

Parathyroid carcinoma as the cause of primary hyperparathyroidism was found in 3 out of 102 patients. The diagnosis was based on the findings of markedly increased serum calcium and parathormone values, definite infiltration of the tumour into the surrounding tissue, mitoses, wide connective tissue septa in the tumour as well as rupture of the capsule and penetration of vessels. The diagnosis can only be made after close cooperation between endocrinologists, surgeons and pathologists.

Adult↗

PubMed1990

Expression of platelet-derived growth factor beta-receptors on stromal tissue cells in human carcinoid tumors.

Carcinoid tumors of the midgut type are slowly growing neoplasms which often present clinically and histologically pronounced fibrosis around the tumors. Cryosections from 41 neuroendocrine tumors (31 midgut carcinoid tumors, 8 endocrine pancreatic carcinomas, 1 parathyroid carcinoma, and 1 pheochromocytoma) and 22 nonneuroendocrine carcinomas were examined for the presence of platelet-derived growth factor (PDGF) beta-receptor by immunohistochemistry using the monoclonal antibody PDGFR-B2. Twenty midgut carcinoid tumor tissues (66%) and 4 endocrine pancreatic carcinomas (50%) and the parathyroid carcinoma stained positively with the antibody. In contrast, only 2 nonneuroendocrine tumor tissues (10%) were stained, and the staining in these cases was weak. The immunoreaction in the carcinoid tumors was observed in connective tissue cells adjacent to tumor cell clusters but not in the tumor cells themselves. The degree of positive PDGF beta-receptor expression in the carcinoid tissues seems to correlate positively with the presence of macrophages as determined by the monoclonal antibody anti-Leu-M5, but not with other infiltrated lymphocytes identified with the monoclonal antibody anti-Leu-4, or with anti-HLA-DR antibodies. Stromal cells adjacent to tumor cells, including small capillaries, stained more strongly than the stromal cells which were distant from tumor cell clusters. Furthermore, carcinoid tumor metastases from lymph nodes as well as from liver showed stronger immunoreactivity in the stromal cells with the PDGF beta-receptor antibody than the corresponding primary tumors. Our data suggest that carcinoid tumor cells may directly or indirectly induce expression of PDGF beta-receptor on adjacent stromal cells in the tumor tissue, which may contribute to the fibrosis that is often seen around carcinoid tumors.

Aged↗

PubMed2006

Synchronous sporadic carcinoma and primary hyperplasia of the parathyroid glands: A case report and review of the literature.

Parathyroid carcinoma is the least common endocrine malignancy. Although it has been noted to be associated with certain clinical factors, such as familial hyper-parathyroidism, its etiology remains unknown. In rare instances, particularly in patients with chronic renal failure, it has been proposed that parathyroid carcinoma can arise from malignant transformation of benign lesions. We present a case of synchronous malignant and primary hyperplastic parathyroid disease in a patient with normal renal function. A 46-year-old woman was seen with symptomatic refractory hypercalcemia. Investigations suggested a hyperactive parathyroid gland. Operative findings were of a low-grade parathyroid carcinoma in concurrence with diffuse hyperplasia of the remaining glands. To our knowledge this represents the fifth reported case. The possibility of malignant change in hyperplastic parathyroid tissue has implications for patient management and follow-up, particularly if tissue is left in situ to maintain hormonal function.

Cell Proliferation↗

PubMed1995

Inactivation of retinoblastoma gene in malignant parathyroid growths: a candidate genetic trigger?

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.

Animals↗

PubMed1991

[Immunohistochemical study of parathyroid hormone related protein (PTHrP) in renal cell carcinoma].

Parathyroid hormone related protein (PTHrP) is the main factor of humoral hypercalcemia of malignancy (HHM). Using anti-PTHrP monoclonal antibody 4B3, we investigated the immunohistochemical localization of PTHrP in human normal renal tissues and renal cell carcinomas. Among normal renal tissues, distal tubules and collecting ducts showed positive immunostaining. Among 36 cases of renal cell carcinoma, PTHrP was detected in 30 cases (83%), and there was no significant correlation between the degree of the immunostaining and the serum calcium levels of the patients. As for the histopathological types of the renal cell carcinomas, granular cell subtypes tended to be more strongly positive than clear cell ones. In conclusion, it was not uncommon that PTHrP was commonly presented by renal cell carcinoma, and HHM occurred when the PTHrP transgressed the homeostatic mechanisms.

Adult↗

PubMed2005

Coherent expression chromosome cluster analysis reveals differential regulatory functions of amino-terminal and distal parathyroid hormone-related protein domains in prostate carcinoma.

Parathyroid hormone-related protein (PTHrP) has a number of cancer-related actions. While best known for causing hypercalcemia of malignancy, it also has effects on cancer cell growth, apoptosis, and angiogenesis. Studying the actions of PTHrP in human cancer is complicated because there are three isoforms and many derived peptides. Several peptides are biologically active at known or presumed cell surface receptors; in addition, the PTHrP-derived molecules can exert effects at the cell nucleus. To address this complexity, we studied gene expression in a DU 145 prostate cancer cell line that was stably transfected with control vector, PTHrP 1-173 and PTHrP 33-173. With this model, regulatory effects of the amino-terminal portion of PTHrP would result only from transduction with the full-length molecule, while effects pertaining to distal sequences would be evident with either construct. Analysis of the expression profiles by microarrays demonstrated nonoverlapping groups of differentially expressed genes. Amino-terminal PTHrP affected groups of genes involved in apoptosis, prostaglandin and sex steroid metabolism, cell-matrix interactions, and cell differentiation, while PTHrP 33-173 caused substantial increases in MHC class I antigen expression. This work demonstrates the distinct biological actions of the amino-terminus compared to distal mid-molecule or carboxy-terminal sequences of PTHrP in prostate carcinoma cells and provides targets for further study of the malignant process.

Journal Article↗

PubMed2005

Parathyroid hormone-related protein in human renal cell carcinoma.

Parathyroid hormone-related protein (PTHrP), a polyprotein discovered in 1987, plays crucial roles not only in development and in various physiological events associated with normal life, but also in a number of pathological conditions such as cancer. PTHrP appears as the major causative agent in humoral hypercalcemia of malignancy (HHM) associated to a broad range of tumors. However, this is only one aspect of the multiple facets of PTHrP in cancer biology. Indeed, the complex growth factor-like properties of PTHrP has shed new light onto potential roles of this peptide in the regulation of tumor growth and invasion. Initial studies in breast, prostate and lung cancer and recent results in renal cell carcinoma (RCC) suggest such roles and highlight the therapeutic potential of PTHrP-targeting strategies in human cancer including RCC. In this review, the role of PTHrP in RCC tumorigenesis and its potential as a therapeutic target will be discussed.

Animals↗

PubMed1999

Parathyroid hormone-related protein as a growth regulator of prostate carcinoma.

Parathyroid hormone-related protein (PTHrP) is produced by prostate carcinoma cells and tumors, but little is known of its role in prostate carcinogenesis. The goal of this study was to evaluate PTHrP expression in the regulation of prostate carcinoma growth using human and animal models. PTHrP expression was assessed in prostate cancer cell lines in vitro. Seven of nine cell lines produced PTHrP, and increased expression was seen during cell proliferation. The MatLyLu rat prostate carcinoma model was used to determine the effects of PTHrP overexpression on prostate tumor growth. PTHrP overexpression did not alter proliferation of the cells in vitro. However, when PTHrP-overexpressing cells were injected into rat hind limbs, primary tumor growth and tumor size were significantly enhanced as compared with control cells. To evaluate PTHrP in human prostate carcinoma patients, immunohistochemistry was performed on metastatic bone lesions. Immunolocalization of PTHrP protein was found in the cytoplasm and nucleus of cancer cells in the bone microenvironment. Because nuclear localization of PTHrP has been associated with an inhibition of apoptosis, the ability of full-length PTHrP to protect prostate cancer cells from apoptotic stimuli was examined. Cells transfected with full-length PTHrP showed significantly increased cell survival after exposure to apoptotic agents as compared with cells producing no PTHrP (plasmid control) or cells transfected with PTHrP lacking its nuclear localization signal. To determine the mechanism of action of PTHrP in prostate cancer cells, the parathyroid hormone/PTHrP receptor status of the cells was determined. These cell lines did not demonstrate parathyroid hormone/PTHrP receptor-mediated binding of iodinated PTHrP or steady-state receptor message by Northern blot analysis, but they did have a detectable receptor message by reverse transcription-PCR analysis. In summary, PTHrP is expressed in many prostate cancer cell lines in vitro and in metastatic bone lesions in vivo. PTHrP expression positively influences primary tumor size in vivo and protects cells from apoptotic stimuli. These data suggest that PTHrP plays an important role in the promotion of prostate tumor establishment and/or progression.

Animals↗

PubMed1992

Large parathyroid functioning carcinoma (1,200 g) presenting as a substernal goiter.

Parathyroid carcinoma is a rare tumor responsible for 0.5-5% of primary hyperparathyroidism. It is usually small (not more than 27 g) and the precise diagnosis of malignancy is made when local or distant metastases are found. We describe a case of a 37 yr old male presenting with a substernal goiter and no specific symptoms except hypertension. This mass had cysts and calcifications and it was in the anterior upper mediastinum. The patient had severe hypercalcemia (Ca greater than 14 mg/dl), high PTH levels and mild renal failure. Bone scanning showed signs of hyperparathyroidism. The patient was subjected to total thyroidectomy and removal of the mass en block. The tumor was circumscribed lobulated and mostly cystic. It weighed 1,200 g (380 g after evacuation of cysts) and measured 12 x 9 x 4.5 cm. Histologic examination showed a highly differentiated adenocarcinoma of parathyroid with metastasis in a regional lymph node. Almost 4 years later the patient is alive and well without hypercalcemia and without evidence of distant metastases.

Adenocarcinoma↗

PubMed1990

Parathyroid hormone related peptide can function as an autocrine growth factor in human renal cell carcinoma.

Parathyroid hormone related peptide (PTHrP) has been implicated in the cause of the hypercalcemia associated with a number of malignant tumours. The data presented here suggests that PTHrP (in addition to its known role of mediating hypercalcemia) may be involved in the autocrine regulation of growth of some tumours. Polyclonal PTHrP antiserum almost totally inhibited the growth of a human renal cell carcinoma cell line, known to secrete PTHrP, in vitro and growth was significantly inhibited by the competitive PTH antagonist PTH (3-34)NH2.

Carcinoma, Renal Cell↗

PubMed2000

[Parathyroid gland carcinoma with postoperative encephalopathy].

We present a 78-year-old patient who suffered from symptomatic transitory psychotic syndrome after laparotomy. Persisting somnolence appeared with cardiopulmonary decompensation and gastrointestinal atony. Due to prolonged hypercalcemia primary hyperparathyreoidism was diagnosed. Resection of a large carcinoma of the parathyroids led to continuous clinical improvement.

Adenoma↗

PubMed2004

Analysis of parathyroid neoplasms by interphase fluorescence in situ hybridization.

Recent studies have indicated that numerical chromosomal abnormalities, including changes in cyclin D1 and p53, may be involved in parathyroid tumorigenesis. We analyzed a series of parathyroid neoplasms with DNA fluorescent probes to evaluate the diagnostic and prognostic utility of numerical abnormalities of chromosomes 1, 6, 9, 11, 13, 15, 17, and 22 and cyclin D1 and p53 gene loci. Interphase fluorescence in situ hybridization (FISH) analysis was performed on paraffin-embedded tissue sections from 15 parathyroid adenomas and 18 parathyroid carcinomas. Directly labeled fluorescent DNA probes for the centromere region of chromosomes 1, 6, 9, 11, 15, and 17, and locus-specific probes for chromosome 22 and chromosome 13 and for cyclin D1 and p53 gene loci were used for dual-probe hybridization. Sixty-seven percent (10 of 15) parathyroid adenomas and 78% (14 of 18) of parathyroid carcinomas showed chromosome gains. Seventy-three percent (11 of 15) of parathyroid adenomas and 33% (6 of 18) of parathyroid carcinomas showed chromosome losses. Normal parathyroid tissues used as controls showed no chromosomal abnormalities. Parathyroid hyperplasias averaged 1.8 gains and 0.2 losses per case. Parathyroid adenomas averaged 2.8 gains and 0.8 losses per case, and parathyroid carcinomas averaged 3.6 gains and 0.6 losses per case. In summary, chromosome abnormalities, both gains and losses, are common in parathyroid adenomas and carcinomas. Parathyroid carcinomas tend to show gains of more chromosome than adenomas. Chromosome 11 was the most frequent chromosome loss identified in parathyroid adenomas and a frequent chromosomal gain in parathyroid carcinomas. These results indicate that gain of chromosome 11 is associated with more aggressive biologic behavior in parathyroid neoplasms.

Adenoma↗

PubMed2004

Azidothymidine induces apoptosis and inhibits cell growth and telomerase activity of human parathyroid cancer cells in culture.

UNLABELLED: Telomerase activity has been correlated to parathyroid carcinoma. Because its role in acquisition of a malignant phenotype by parathyroid cells is unclear, we treated telomerase-positive cultured human parathyroid cancer cells with the telomerase inhibitor AZT, evaluating cell telomerase activity, cytotoxic effects, growth, and morphological changes. In vitro exposure of these cells to AZT correlated with inhibition of cell proliferation. INTRODUCTION: Parathyroid carcinoma represents an uncommon cause of primary hyperparathyroidism, whose spectrum of clinical presentation, degree of malignancy, and prognosis are difficult to be properly identified. Neck surgery, specifically an en bloc resection of primary tumor, is the only curative treatment. Alternatively, affected patients could undergo repetitive palliative surgical exeresis of metastatic nodules. It has been previously shown that telomerase activity is specifically present in parathyroid carcinoma cells, being absent in hyperplastic and adenomatous tissues. Thus, determination of telomerase activity could represent either a useful diagnostic molecular marker for human parathyroid carcinoma or a potential target for pharmacological intervention in a malignant neoplasia usually resistant to chemo- and radiotherapeutic interventions. MATERIALS AND METHODS: To further investigate the role of telomerase activity in acquisition of a malignant phenotype by parathyroid cells, we treated telomeric repeat amplification protocol-positive cultured human parathyroid cells with the telomerase inhibitor zidovudine, 3'-azido-3'deoxythymidine (AZT), evaluating cell telomerase activity, growth characteristics, potential cytotoxic effects, and morphological changes. RESULTS: Our findings indicate that in vitro exposure of human parathyroid cancer cells to AZT resulted in intracellular accumulation of AZT-monophosphate (AZT-MP) and inhibition of telomerase, which correlate with inhibition of human parathyroid cancer cell proliferation. Moreover, we also found that AZT induced an apoptotic rather than a necrotic type of cellular death. None of these effects were observed in human adenomatous parathyroid cells in culture. CONCLUSIONS: Altogether these results indicate that AZT may be a highly effective agent against cancer parathyroid cells proliferation, which is an extremely important observation for a neoplasia which shows lack of response to classical pharmacological and physical antiblastic treatments.

Aged↗

PubMed1995

Endocrine malignancies that may mimic benign lesions.

A variety of malignant tumors that occur in endocrine organs may mimic benign lesions histologically. In this article, a number of such tumors are selected for discussion, including several variants of papillary thyroid carcinoma (encapsulated follicular, diffuse sclerosing, diffuse follicular, macrofollicular, cystic, and stroma-rich), paucicellular anaplastic thyroid carcinoma, primary thyroid low grade B-cell lymphoma of mucosa-associated lymphoid tissue type, adrenocortical carcinoma, and parathyroid carcinoma. Emphasis is placed on the histological clues that are helpful for recognizing the malignant nature of these lesions.

Adenoma↗

PubMed1996

Allelic loss of the retinoblastoma tumor suppressor gene: a marker for aggressive parathyroid tumors?

Allelic loss of the retinoblastoma tumor suppressor gene has recently been shown to be highly specific for parathyroid carcinoma. It has been proposed that this genetic abnormality may have diagnostic and prognostic implications for parathyroid carcinoma, but to date no further studies are available to substantiate these findings. In the present study, three cases of atypical recurrent hyperparathyroidism were examined: a patient with parathyroid carcinoma and an autotransplanted adenoma that progressed into carcinoma, a patient with recurrent juvenile hyperparathyroidism, and a patient with severe recurrent secondary hyperparathyroid disease due to rapidly growing autotransplant. Six pairs each of sporadic parathyroid adenoma and secondary parathyroid disease were also studied for comparison. Allelic losses of RB and D13S71 at 13q14 was found in the parathyroid carcinoma and the corresponding autotransplant that had previously been considered benign tissue and in the case of recurrent juvenile hyperparathyroidism, but not in any of the other tumors. Our findings support the findings of the previous study that RB or 13q loss is specific for parathyroid tumors with increased aggressiveness and might be of clinical significance.

Adenoma↗