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PubMed1999

Recurrent clear cell carcinoma of the ovary changing into producing parathyroid hormone-related protein (PTH-rP) with hypercalcemia.

We experienced the case of a clear cell carcinoma of the ovary arising from an endometrial cyst, which started to produce parathyroid hormone-related protein (PTH-rP) in a recurrent tumor, thus inducing hypercalcemia. Using immunohistochemical analysis, we demonstrated that the primary carcinoma was immunonegative for PTH-rP, but that the recurrent carcinoma was strongly immunopositive for PTH-rP.

Adenocarcinoma, Clear Cell↗
PubMed1989

Immunocytochemical localization of vitamin D-dependent calcium-binding protein (calbindin) in thyroid parafollicular cells of guinea pig.

The presence of the 28K vitamin D-dependent, calcium-binding protein (28K calbindin) was investigated by immunocytochemistry in normal thyroid glands and parathyroid glands of rats, guinea pigs, rabbits and men, as well as in human thyroid medullary carcinomas and human parathyroid adenomas. In addition, thyroid glands and parathyroid glands of rats and guinea pigs were studied after treatment with vitamin D3 injected intramuscularly at a total dose of 1.2 x 10(6) IU per 100 g body weight. 28K calbindin was found exclusively in parafollicular cells of guinea pigs and never in those of other species investigated. It was present predominantly in the cytoplasm and in lower concentration in nuclei. After vitamin D3 treatment, increased immunoreactivity of 28K calbindin was observed in the cytoplasm and, even more pronounced, in the nuclei. In normal parathyroid cells and in parathyroid tumors and medullary thyroid carcinomas, 28K calbindin was not demonstrable. Our findings suggest an important function of calbindin in the cellular calcium processing of parafollicular cells of guinea pigs.

Adenoma↗
PubMed1993

In situ localization of parathyroid hormone-like protein and mRNA in intraepithelial neoplasia and invasive carcinoma of the uterine cervix.

Parathyroid-like protein (PLP), or parathyroid hormone-related peptide, is a well-recognized mediator of paraneoplastic hypercalcemia (humoral hypercalcemia of malignancy syndrome). In this study we examined the expression of PLP by 40 invasive squamous cell carcinomas (SCCs) of the cervix and selected carcinomas of nonsquamous histology. Using a polyclonal antibody to human PLP, 93% of SCCs, including two tumors from patients with humoral hypercalcemia of malignancy syndrome, showed moderate to strong cytoplasmic immunoperoxidase staining for PLP. The strongest staining often was observed in areas of invasion associated with stromal desmoplasia. The small number of weak or negatively stained SCCs were all poorly differentiated tumors. Although native uninvolved squamous epithelium showed weak to moderate staining of the superficial layers, there was variable or full-thickness immunostaining in areas of dysplasia. Normal endocervical glands and stroma as well as cervical adenocarcinomas and neuroendocrine carcinomas were negative. In situ hybridization studies showed abundant PLP mRNA within SCC in patients with hypercalcemia. However, PLP mRNA was of relatively low abundance in tumors of normocalcemic patients. Ultrastructural studies showed cytoplasmic, membrane-bound, granular inclusions in tumor cells from the hypercalcemic patients. Our data suggest that increased PLP gene transcription contributes to the increased production of PLP and the pathogenesis of humoral hypercalcemia of malignancy syndrome.

Adult↗
PubMed1975

Subcutaneous bone formation in the naevoid basal-cell carcinoma syndrome: normal urinary cyclic AMP response to parathyroid hormone infusion.

A patient with the naevoid basal-cell carcinoma syndrome had subcutaneous bone formation in the areas other than those occupied by the carcinomata. The patient did not show a significant phosphaturic response after parathyroid hormone infusion, but this extract produced a normal excretion of cyclic AMP. This proves that the subcutaneous bone does not signify an affinity to pseudo-hypoparathyroidism.

Adult↗
PubMed1996

Molecular genetics of hyperparathyroid disease.

Information on genetic abnormalities in primary hyperparathyroidism has accumulated gradually. Genetic alterations responsible for tumorigenesis have been identified in multiple endocrine neoplasia types 1 and 2. Point mutations in a calcium-sensing receptor gene were recently found to be responsible for familial hypocalciuric hypercalcaemia and neonatal severe hyperparathyroidism. Evidence has been provided that abnormalities of cell cycle regulation participate at tumorigenesis in parathyroid adenoma and carcinoma. Clonal analysis has shown that in renal hyperparathyroidism the parathyroid glands initially grow diffusely and polyclonally, after which foci of nodular hyperplasia are transformed to monoclonal neoplasia. Somatic changes of specific genes have been suspected of being responsible for parathyroid tumorigenesis in renal hyperparathyroidism. However, the genetic loci responsible for the frequent monoclonality largely remain to be identified, and heterogeneous genetic abnormalities may contribute to the progression of secondary parathyroid hyperplasia.

Adenoma↗
PubMed2004

Cdx2 as a marker for neuroendocrine tumors of unknown primary sites.

The transcription factors CDX1 and CDX2 are homeobox genes that regulate development of the epithelium of the small and large intestine. A few studies have shown that Cdx2 protein expression is useful in the diagnosis of adenocarcinomas as well as neuroendocrine tumors of the small and large intestine. To examine the utility of Cdx2 in recognizing neuroendocrine tumors of unknown primary sites, we analyzed 224 primary and metastatic neuroendocrine tumors by immunohistochemistry. The specificity of the antibody reaction was confirmed by Western blotting. Cdx2 antibody stained all primary and most metastatic midgut carcinoid tumors. A few rectal and pulmonary carcinoids were positive, while gastric carcinoids were negative for Cdx2. One of five small cell carcinomas (20%) of the colon was positive for Cdx2, while all pulmonary small cell carcinomas were negative. Neuroendocrine tumors of the pituitary, parathyroid, medullary thyroid carcinomas, paragangliomas, pheochromocytomas and Merkel cell carcinomas were all negative for Cdx2. Western blot analysis of seven cases showed a 40 kDa band in both primary and metastatic midgut carcinoid tumors. These results indicate that Cdx2 can be very useful in recognizing metastatic neuroendocrine carcinomas of unknown primary sites, especially when they are derived from the small intestine.

Biomarkers, Tumor↗
PubMed1979

Pituitary adenoma, primary parathyroid hyperplasia and papillary (non-medullary) thyroid carcinoma. A case of multiple endocrine neoplasia (MEN).

An acidophilic pituitary adenoma associated with primary nodular parathyroid hyperplasia and a small papillary thyroid carcinoma was discovered at the autopsy of a 44 year old female acromegalic. The thyroid carcinoma showed evidence of lymphatic spread. Several etiopathogenetic mechanisms for the non-medullary thyroid carcinomata associated with Multiple Endocrine Neoplasia (MEN) have been postulated, since the follicular epithelium of the thyroid does not belong to the neural ectoderm derivates unlike the C-cells of the thyroid, the adenohypophysis and probably the parathyroid glands. Apart from genetic influence, or coincidence, one has to rule out carcinogenic exposure or hormonal influence. Clinically speaking, one should always consider whether malignant thyroid disease coexists with hyperplastic or neoplastic parathyroid tissue.

Adenoma, Acidophil↗
PubMed2003

HRPT2 mutations are associated with malignancy in sporadic parathyroid tumours.

BACKGROUND: Hyperparathyroidism is a common endocrinopathy characterised by the formation of parathyroid tumours. In this study, we determine the role of the recently identified gene, HRPT2, in parathyroid tumorigenesis. METHODS: Mutation analysis of HRPT2 was undertaken in 60 parathyroid tumours: five HPT-JT, three FIHP, three MEN 1, one MEN 2A, 25 sporadic adenomas, 17 hyperplastic glands, two lithium associated tumours, and four sporadic carcinomas. Loss of heterozygosity at 1q24-32 was performed on a subset of these tumours. RESULTS: HRPT2 somatic mutations were detected in four of four sporadic parathyroid carcinoma samples, and germline mutations were found in five of five HPT-JT parathyroid tumours (two families) and two parathyroid tumours from one FIHP family. One HPT-JT tumour with germline mutation also harboured a somatic mutation. In total, seven novel and one previously reported mutation were identified. "Two-hits" (double mutations or one mutation and loss of heterozygosity at 1q24-32) affecting HRPT2 were found in two sporadic carcinomas, two HPT-JT-related and two FIHP related tumours. CONCLUSIONS: The results in this study support the role of HRPT2 as a tumour suppressor gene in sporadic parathyroid carcinoma, and provide further evidence for HRPT2 as the causative gene in HPT-JT, and a subset of FIHP. In light of the strong association between mutations of HRPT2 and sporadic parathyroid carcinoma demonstrated in this study, it is hypothesised that HRPT2 mutation is an early event that may lead to parathyroid malignancy and suggest intragenic mutation of HRPT2 as a marker of malignant potential in both familial and sporadic parathyroid tumours.

Adult↗
PubMed2002

Hypercalcemia induced by parathyroid hormone-related peptide after treatment of carcinoma.

Squamous cell carcinoma of the head and neck is a rare cause of humoral hypercalcemia of malignancy. This paraneoplastic syndrome is usually one of the presenting symptoms of the disease. We report a case of squamous cell carcinoma of the oral cavity that presumably elaborated parathyroid hormone-related peptide (PTH-rP) and caused hypercalcemia only after radiotherapy and chemotherapy.

Aged↗
PubMed2003

Serum levels of angiogenic growth factors in patients with thyroid gland tumors and parathyroid adenoma.

OBJECTIVE: Angiogenic growth factors bFGF and VEGF ensure vascularisation of the growing tumor tissue. We decided to investigate their peripheral serum concentrations in patients with thyroid gland adenoma and papillary carcinoma and with parathyroid adenoma. We wanted to find the possible serum marker of these tumor diseases. METHODS: 28 patients with thyroid gland tumor (14x adenoma, 14x papillary carcinoma) and 12 patients with parathyroid gland adenoma. Growth factors serum levels were measured by ELISA method. RESULTS: We found significantly higher serum levels of bFGF in both groups of patients with thyroid adenoma (4.93 +/- 3.42 ng/ml) and papillary carcinoma (5.69 +/- 5.58 ng/ml) compared to the healthy population (1.47 +/- 1.77 ng/ml). There were no significant differences of VEGF serum levels between all examined groups of patients (adenoma 213 +/- 197, papillary carcinoma 210 +/- 179, healthy 227 +/- 231 pg/ml). We found significantly higher serum levels of bFGF in patients with parathyroid gland adenoma (7.59 +/- 9.12 ng/ml) compared to those in healthy people (1.47 +/- 1.77 ng/ml). CONCLUSIONS: Higher bFGF serum concentrations in patients with thyroid and parathyroid tumors are in accordance with their immunohistochemical tissue levels described in the literature. Not so in VEGF. bFGF may be a serum marker of thyroid and parathyroid neoplasms.

Adenoma↗
PubMed1983

[Parathyroid gland cancer and hyperparathyroidism].

A patient with an endocrine-active carcinoma of the parathyroid gland was observed. The typical signs of hyperthyroidism could be seen in the skeletal system. Symptoms of bone and kidney diseases dominated the clinical picture. The symptomatology corresponded to a subchronic primary hyperparathyroidism.

Adenocarcinoma↗
PubMedDate not supplied

[A patient with MEN-IIA syndrome due to de novo mutation and papillary thyroid carcinoma; the role of 99m Tc-depreotide in diagnosing metastases and brief review of the literature].

Multiple endocrine neoplasia syndrome type II-A (MEN-IIA) is a rare endocrinological disorder occurring in 0.04% of the general population. The combination of papillary thyroid carcinoma with MEN-IIA appears even less frequently. We describe the case of a 21-year-old woman with pheochromocytoma of the left adrenal gland, medullary thyroid carcinoma, hyperplasia of the parathyroid glands and papillary thyroid carcinoma. MEN II-A syndrome resulted from de novo mutation of the RET proto-oncogene, which was detected in the DNA of peripheral blood leucocytes. Three months postoperatively calcitonin levels were normal, whilst increased serum thyroglobulin values prompted the need for further investigation. Whole body scanning with (131)I and with (99m)Tc-sestamibi and also US test of cervical lymph nodes, were negative. The synthetic analogue of somatostatin (99m)Tc-depreotide was used for whole body scintigraphy, cervical and thoracic tomographic scanning and revealed anterior cervical, upper mediastinal and right hilar foci of pathological uptake[Fig.1 and Table 1: see text]. These findings were compatible with findings from CT and MRI that followed in order to complete the diagnostic evaluation. The patient underwent surgical resection of the metastatic foci with uneventful postoperative course. Histology showed lymph node metastases originating from the papillary thyroid carcinoma. Ratio values >2 were abnormal (Fig. 2). Computer processing of the corresponding ROIs on healthy tissues produced the following normal values: Th/Arm: 1.874,, Med/Arm: 1.699, Hi/Arm: 1.141 (Fig. 3).

English Abstract↗
PubMed1998

Regulation of parathyroid hormone-related protein expression in a canine squamous carcinoma cell line by colchicine.

The regulation of parathyroid hormone-related protein expression by colchicine, vinblastine, nocodazole, taxol, transforming growth factor-beta1 (TGFbeta1), and epidermal growth factor (EGF) was investigated in a canine squamous carcinoma cell line (SCC 2/88 cells). SCC 2/88 cells were stably transfected with a human P2/P3 PTHrP promoter-luciferase reporter gene construct and gene expression was measured after chemical treatments. The greatest increase in reporter gene expression was observed after colchicine treatment and small increases occurred after treatment with vinblastine, taxol, TGFbeta1, or EGF. Nocodazole had no significant effect on reporter gene expression. Colchicine also increased PTHrP steady state mRNA expression and PTHrP secretion by SCC 2/88 cells. These results demonstrated that PTHrP production was increased in SCC 2/88 cells by colchicine and suggested that factors or events during mitosis are capable of stimulating PTHrP production. An increase in PTHrP production during mitosis of malignant epithelial cells may be important in the pathogenesis of humoral hypercalcemia of malignancy.

Animals↗
PubMed2005

Primary parathyroid tumors of the mediastinum: a clinicopathologic and immunohistochemical study of 17 cases.

We describe 17 cases (9 women, 8 men; aged 36 to 72 years) of primary parathyroid tumors occurring primarily in the anterior mediastinum. Clinically and radiologically, all patients had an anterior mediastinal tumor. All patients had metabolic disturbances with calcium and phosphorus. Of 17 patients, 13 had clinical primary hyperparathyroidism, 1 had secondary hyperparathyroidism due to polycystic kidney disease, and 1 had a history of prostatic carcinoma and 1 of chronic obstructive pulmonary disease. In 1 patient, the tumor was found at autopsy. Grossly, the tumors varied in size from 2 to 7 cm in greatest dimension. Histologically, 2 tumors showed features of parathyroid carcinoma, and 15 tumors showed more conventional features of parathyroid adenomas. Six tumors were predominantly oncocytic, 6 were composed predominantly of chief cells, and 3 had mixed cellular composition. Immunohistochemical studies for chromogranin, synaptophysin, low-molecular-weight keratin (CAM 5.2), and parathyroid hormone were performed in 10 cases (8 parathyroid adenomas and 2 parathyroid carcinomas). All the tumors examined showed variable positive reaction for those antibodies. The cases highlight the importance of keeping primary parathyroid tumors in the differential diagnosis of anterior mediastinal tumors.

Adult↗