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PubMed1976

Adrenal medullary disease in multiple endocrine neoplasia, type 2: pheochromocytoma and its precursors.

Multiple endocrine neoplasia, type 2 (MEN-type 2), designates the syndrome of medullary thyroid carcinoma, pheochromocytoma, and occasional parathyroid hyperplasia. The thyroid carcinoma, which is usually bilateral and multicentric, is preceded by multifocal C-cell hyperplasia. The adrenal gland manifests pheochromocytoma, which is frequently bilateral and multicentric, and may be malignant. To test the hypothesis that diffuse adrenal medullary hyperplasia is a precursor of pheochromocytoma in this syndrome, we studied the adrenal glands of 19 patients who had MEN-type 2. The findings in the adrenal medulla in these 19 patients were: synchronous bilateral pheochromocytoma in 9 (metastatic in 3); asynchronous bilateral pheochromocytoma in 1 (metastatic); unilateral pheochromocytoma with contralateral diffuse and nodular hyperplasia in 2; unilateral pheochromocytoma with contralateral diffuse hyperplasia in 2; unilateral pheochromocytoma in 1; bilateral nodular hyperplasia in 1; bilateral diffuse hyperplasia in 1; and no abnormality in 2. This spectrum of adrenal medullary pathology suggests that diffuse and nodular medullary hyperplasia are precursors of pheochromocytoma in MEN-type 2.

Adrenal Gland Neoplasms↗
PubMed1992

A kindred of multiple endocrine neoplasia type 2B.

We describe familial cases of multiple endocrine neoplasia (MEN) 2B: A 48-year-old man is the proband. He had pheochromocytoma, medullary thyroid carcinomas (MTCs), parathyroid hyperplasia, mucosal neuromas, eversion of eyelids and Marfanoid appearance, and then underwent adrenalectomy and total thyroidectomy. Family screening revealed that his two daughters (10 and 8 years old) had mucosal neuromas and increased serum calcitonin (CT). Both of them had MTCs but no pheochromocytoma, and their MTCs were surgically removed. The father and his children have been in favorable condition since the operations. Southern blot analysis with 33 polymorphic DNA probes was done in MTCs obtained from two daughters. An RBP3 (10q11.2) locus linked to a predisposing gene on chromosome 10 was uninformative in either patient because of constitutional homozygosity. Loss of heterozygosity at the MYCL1 locus on chromosome 1p32 was observed in MTC from the younger sister, but no loss of heterozygosity was recognized in other loci examined. Deletion of the 1p32 locus may play a role in the development of MEN 2B.

Adrenal Gland Neoplasms↗
PubMed1991

Flow cytometric DNA analysis of normal and pathologic parathyroid glands.

Assessment of cellular DNA content and cell cycle analysis by flow cytometry has been useful in predicting patient survival and the malignant potential of many neoplasms. In this study, we analyzed the DNA content and cell cycle distribution of 12 parathyroid adenomas, 15 carcinomas, 5 secondary hyperplasias, and 14 normal parathyroid glands. Appropriate areas demonstrating the pathologic changes were dissociated from paraffin-embedded, formaldehyde-fixed tissue for this purpose. All the cells from normal glands were diploid with mean and median S-phase fractions of 1.2% (range, 0.3-2.7%). Of the 18 glands from five patients with secondary hyperplasia, 4 (22%) had some cells which were aneuploid (from three patients), and 14 (78%) had only cells with a diploid DNA content. Mean and median S-phase fractions were 0.8% (range, 0.3-1.5%). One (8%) of the adenomas was tetraploid, 3 (25%) were aneuploid, and 8 (67%) were diploid. The mean S-phase fraction was 1.5% (range, 0.3-3.8%). Four (27%) of the carcinomas had tetraploid cells, 6 (40%) had aneuploid cells, and 5 (33%) had only diploid cells. Carcinomas had a mean S-phase fraction of 6.0% (median, 5.3%; range, 1.4-14.1%). This study indicates that DNA aneuploidy or tetraploidy may be present in many abnormal parathyroid entities, but not in normal parathyroids. Proliferative activity when considered with the DNA index may be a helpful adjunct in separating carcinomas from adenomas or hyperplasias.

Adenoma↗
PubMed2004

Coexistent thyroid pathologies and high rate of papillary cancer in patients with primary hyperparathyroidism: controversies about minimal invasive parathyroid surgery.

Thyroid carcinoma and benign thyroid diseases associated with primary hyperparathyroidism (PHPT) may cause difficulties in the diagnosis, localization and therapy of PHPT. In this study, we analysed coexistent thyroid pathologies in 51 patients who underwent neck exploration with a diagnosis of PHPT between 1999--2002. Five hundred thirteen patients who underwent thyroidectomy for nodular thyroid disease without a parathyroid pathology in histopathological examination served as controls. In patients with PHPT there were 43 cases (84.3%) of coexistent thyroid pathology. Nine patients (17.6 %) had coexistent papillary thyroid cancer. Nine patients (17.6 %) had lymphocytic thyroiditis, two (3.9%) had benign thyroid adenoma and 24 (47%) had nodular hyperplasia. In one patient (2%), there was intrathyroidal metastasis from a parathyroid cancer. One patient had coexistent lymphocytic thyroiditis and multifocal papillary cancer. One of the two cases with thyroid adenomas was Hürthle cell type. In the control group only 28 patients (5.5%) had thyroid malignancy (27 papillary cancer and one follicular cancer). In conclusion, the coexistent thyroid pathologies are highly prevalent in patients with PHPT and pre- and intra-operative thyroid examination should be performed to avoid overlooking important thyroid pathologies.

Adolescent↗
PubMed1988

Human renal carcinoma expresses two messages encoding a parathyroid hormone-like peptide: evidence for the alternative splicing of a single-copy gene.

A peptide secreted by tumors associated with the clinical syndrome of humoral hypercalcemia of malignancy was recently purified from human renal carcinoma cell line 786-0. The N-terminal amino acid sequence of this peptide has considerable similarity with those of parathyroid hormone (PTH) and of peptides isolated from human breast and lung carcinoma (cell line BEN). In this study we obtained the nucleotide sequence of a 1595-base cDNA complementary to mRNA encoding the PTH-like peptide produced by 786-0 cells. The cDNA contains an open reading frame encoding a leader sequence of 36 amino acids and a 139-residue peptide, in which 8 of the first 13 residues are identical to the N terminus of PTH. Through the first 828 bases the sequence of this cDNA is identical with one recently isolated from a BEN cell cDNA library; however, beginning with base 829 the sequences diverge, shortening the open reading frame by 2 amino acids. Differential RNA blot analysis revealed that 786-0 cells express two major PTH-like peptide mRNAs with different 3' untranslated sequences, one of which hybridizes with the presently described sequence and the other one with that reported for the BEN cell PTH-like peptide cDNA. Primer-extension analysis of 786-0 poly(A)+ RNA together with Southern blot analysis of human DNA confirmed the presence of a single-copy gene coding for multiple mRNAs through alternate splicing. In addition, the 3' untranslated sequence of the cDNA described here has significant similarity to the c-myc protooncogene.

Amino Acid Sequence↗
PubMed2003

The parathyroid hormone-related protein receptor is expressed in breast cancer bone metastases and promotes autocrine proliferation in breast carcinoma cells.

Overproduction of parathyroid hormone-related protein (PTHRP) occurs in a high proportion of primary breast cancers (PBC) and is strongly implicated in their metastatic spread to bone. Although the PTHRP-receptor (PTHRP-R) is often coexpressed with PTHRP in PBC, its role in regulating breast cancer cell proliferation and metastases to bone remains unclear. The aims of this study were to determine the expression of the PTHRP-R in breast cancer bone metastases (BM) and to investigate the effects of PTHRP-R overexpression on breast cancer cell proliferation. PTHRP-R expression occurred in 85% (11 out of 13) of BM compared with 58% (39 out of 67) of PBC. Median expression was higher (P<0.05) in BM compared with PBC. PTHRP increased cAMP accumulation and DNA synthesis in MCF-7 cells stably overexpressing the PTHRP-R (MCF-7(WTR)) but not in MCF-7(VEC) control cells. The increase in DNA synthesis was mimicked by the cAMP pathway activator forskolin. The receptor antagonist PTHRP(7-34) reduced DNA synthesis in MCF-7(WTR) cells, but not MCF-7(VEC) cells, indicating that receptor overexpression promotes autocrine PTHRP activity. MCF-7(WTR) cells showed increased mitogenic responsiveness to fetal calf serum and reduced doubling times. PTHRP induced weak activation of ERK1 and ERK2 and potentiated their activation by serum growth factors. Collectively these results show that the PTHRP-R is frequently expressed in breast cancer BM and indicate that receptor overexpression drives proliferation via autocrine signals that are mediated via cAMP and ERK pathways.

Autocrine Communication↗
PubMed1995

Three cases of primary hyperparathyroidism associated with nonmedullary thyroid carcinoma.

Nonmedullary thyroid carcinoma was diagnosed in three of nine cases of primary hyperparathyroidism. In all three cases, diagnosis of primary hyperparathyroidism was made before that of thyroid carcinoma. In the first case, follicular carcinoma was incidentally detected during parathyroidectomy. In the second case, thyroid tumor was discovered during imaging studies for hyperparathyroidism. Papillary carcinoma and ectopic parathyroid was diagnosed postoperatively. In the third case, a thyroid lesion had been mistaken for a putative parathyroid lesion, but the diagnosis of papillary carcinoma was obtained. These cases suggest that preoperative examination for hyperparathyroidism should be carefully evaluated, considering possible concomitant thyroid lesions.

Adenocarcinoma↗
PubMed2003

Humoral hypercalcemia of malignancy due to bipartite squamous cell/small cell carcinoma of the esophagus immunoreactive for parathyroid hormone related protein.

We report the case of a 63-year-old man who presented with weakness, fatigue, dehydration, confusion, abdominal pain, congestive heart failure and hypercalcemia. He expired and autopsy revealed an exulcerating carcinoma of the esophagus, invading the esophageal wall and metastasizing to the lungs, skin and lymph nodes. Histology demonstrated an epithelial tumor consisting of two components with transition between the two. One component was a keratinizing squamous cell carcinoma, whereas the other component consisted of pleomorphic small cells. The hypercalcemia was assumed to be due to parathyroid hormone related protein (PHRP), which was demonstrated by immunohistochemistry only in the pleomorphic small cells and not in the squamous cells. PHRP induced humoral hypercalcemia of malignancy is most often associated with squamous cell carcinomas. The finding that in our case, the pleomorphic small cell component was PHRP immunopositive and the squamous cell component showed no immunoreactivity, is intriguing and remains unexplained.

Carcinoma, Small Cell↗
PubMedDate not supplied

Feline head and neck squamous cell carcinoma cell line: characterization, production of parathyroid hormone-related protein, and regulation by transforming growth factor-beta.

A natural animal model for human head and neck squamous cell carcinoma (H/N SCC) has not been described. The domestic cat has a high spontaneous occurrence of oropharyngeal SCC, which is similar to the human disease in aggressiveness and incurability. We have developed a cell line (SCCF1) from a laryngeal SCC of a cat. Keratinocytes were maintained in culture for greater than 50 passages. SCCF1 had strong cytokeratin immunohistochemical staining, weak vimentin staining, and no p53 staining. Ultrastructual features included cytokeratin filaments and desmosomes, as well as features of anaplasia (irregular cytoplasmic and nuclear margins, surface filopodia, and abnormal intermediate filament production). Karyotype analysis revealed aneuploidy, with a stemline chromosomal number of 34. The cells grew logarithmically for 6 d until confluency. SCCF1 expressed parathyroid hormone-related protein (PTHrP) messenger ribonucleic acid (mRNA) and protein, and secreted the protein into the medium. Treatment of SCCF1 with transforming growth factor-beta increased PTHrP production but did not affect PTHrP mRNA stability. Reverse transcriptase-polymerase chain reaction was used to amplify a 282-base pair region of feline PTHrP mRNA, encoding portions of the pre-pro and coding regions. The complementary deoxyribonucleic acid (cDNA) was cloned and sequenced. The cDNA and the predicted amino acid sequences had a high degree of homology to human and canine PTHrP. RT-PCR was used to confirm alternate splicing of PTHrP mRNA for translation of PTHrP 1-139 and PTHrP 1-141. The SCCF1 cell line will permit mechanistic experiments on genetic dysregulation in neoplastic keratinocytes of the feline oropharynx, and development of an in vitro model for H/N cancer.

Alternative Splicing↗
PubMed1989

Primary hyperparathyroidism and coexisting hyperthyroidism--review of the literature.

Concomitance of hyperthyroidism and hyperparathyroidism is rare and only forty-nine well documented cases could be found in the literature. In the present study, only forty-three patients with adequate available clinical and laboratory data are reported. Hypercalcemia was found in all the patients and five of them (12%) had acute hyperparathyroidism. Two patients were also pregnant and had pancreatitis. Hypercalcuria was found in 73% and hypophosphatemia in 55% of the patients. Eleven patients (26%) had renal concretions. Skeletal roentgenograms showed abnormalities in 63% of the patients. Elevated serum level of alkaline phosphatase was present in 64% of the patients. However, there seemed to be no correlation with the severity of the skeletal lesions. Thyrotoxicosis commenced before that of Hyperparathyroidism in twenty-three patients (53%) whereas in the remaining twenty patients it was impossible to determine which disease began first. The etiologies of hyperparathyroidism as well as the differential diagnosis of parathyroid-related and nonparathyroid-related hypercalcemia are discussed. Microscopically, 74% of the patients had a single adenoma; 16% had hyperplasia of one to three parathyroid glands. One patient had an adenoma in combination with hyperplasia of one parathyroid gland, one had an adenoma and three hyperplastic glands, one had adenomas of two parathyroid glands in combination with hyperplasia of one parathyroid gland, and the other one had carcinoma of a parathyroid gland.2+ Finally, if a thyrotoxic patient still has hypercalcemia when becoming euthyroid after antithyroid therapy, coexisting hyperthyroidism should be considered and an operation should be performed as surgical treatment cured both diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1977

[A case of primary hyperparathyroidism sustained by parathyroid adenocarcinomatosis].

Primary hyperparathyroidism may at times be associated with carcinoma of the parathyroids. A personal case of primary hyperparathyroidism was operated on by total thyro-parathyroidectomy. The histological picture presented atypical cell patterns and infiltrations of the thyroid capsule, together with adenomatuous parathyroid formations suggesting the possibility of a malignant transformation of initially benign process. Given the benign clinical course, it is possible that when subjected to radical, timely measures, even atypical parathyroid processes may be cured completely.

Adenocarcinoma↗
PubMed1998

A comparative study of p53 immunoexpression in parathyroid hyperplasias secondary to uremia, primary hyperplasias, adenomas and carcinomas.

OBJECTIVE: To investigate immunoexpression of p53 in parathyroid tumors and hyperplasias and correlate it with the histopathological diagnosis and severity of hyperparathyroidism. DESIGN: A total of 102 parathyroid tissues from archival paraffin-embedded specimens or obtained at surgery between 1988 and 1997 from 65 consecutive individuals with hyperparathyroidism were studied. METHODS: p53 immunoexpression, gland mass, preoperative serum calcium and intact parathyroid hormone (PTH) were analyzed; 14 normal parathyroid glands were used as controls. RESULTS: The histopathological findings were: adenomas (n = 28), primary hyperplasias (n = 12), secondary nodular and diffuse hyperplasias (patients with uremia, n = 57), carcinomas (n = 4) and carcinomatous metastatic tissue (n = 1). Nuclear p53 was detected in 36% of the adenomas, 42% of the primary hyperplastic glands, 72% of the diffuse hyperplasias, 44% of nodular hyperplasias and 40% of the carcinomatous tissues, and was absent from normal glands. p53 expression was significantly more frequent in diffuse hyperplasias than in adenomas (P = 0.037). Serum ionized calcium tended to be higher in p53-positive glands in all histopathological groups; however, the difference was only significant in nodular hyperplasias (P = 0.018). The same trend was observed for serum intact PTH levels of adenomas and nodular hyperplastic glands. Gland mass was not significantly different according to p53 staining. CONCLUSIONS: p53 immunoexpression was not useful in differentiating between the histopathological parathyroid subgroups. p53 immunodetection was particularly frequent in secondary hyperplastic glands of uremic patients. Our study suggests that p53, whether wild-type or mutant, is regulated in parathyroid tumors and hyperplasias. Changes in wild-type p53 may be part of a cellular response to a hyperproliferative condition.

Adenoma↗
PubMed1990

Flow cytometric DNA analysis of parathyroid tumors. Implication of aneuploidy for pathologic and biologic classification.

The previous cytometric studies on parathyroid tumors have provided conflicting data regarding the relationship between DNA content and histopathology, resulting from differences in technical methods and data analysis. This study measured nuclear DNA of parathyroid tumors by flow cytometry in fresh material and determined whether DNA aneuploidy really assists in making a pathologic diagnosis of carcinoma or not. From May 1987 through April 1989, 65 consecutive patients operated on for primary hyperparathyroidism had DNA analysis of the freshly excised parathyroid tumors. Three of the patients had metastatic lesions of parathyroid carcinoma in the lung, cervical lymph nodes, and lung and mediastinal lymph nodes, respectively. Pathologic classifications of the lesions from the other 62 patients were 54 adenomas, four carcinomas, and four hyperplasias. In all the latter patients, hyperplasia was associated with a multiple endocrine neoplasia syndrome. Unequivocal evidence of aneuploidy was found in all of the metastatic lesions and 60% of the primary lesions of the carcinomas, in 9% of the adenomas and in 50% of the hyperplasias. Therefore, parathyroid carcinomas were more apt to be aneuploid than were adenomas (P = 0.0015, both-sided testing). In each of the cases of aneuploid hyperplasia, a small aneuploid peak was found. The high incidence of aneuploidy in patients with multiple endocrine neoplasia type 1 may indicate the presence of clonal heterogeneity of hyperplastic glands and the presence of an abnormal subset of cells that have malignant potential. Cell distribution analysis did not provide any significant information beyond ploidy level. In conclusion, DNA flow cytometric analysis of DNA ploidy patterns is a valuable adjunct to the histopathologic diagnosis of parathyroid neoplasms.

Adenoma↗
PubMed1998

Parathyroid-hormone-related-protein-producing thymic carcinoma presenting as a giant extrathoracic mass.

A 53-year-old female with a 9-month history of chest pain presented with a giant anterior chest wall mass. Radiologic examination showed an anterior mediastinal tumor invading the chest wall. Serum calcium and parathyroid hormone-related protein (PTHrP) levels were extremely elevated. Biopsy specimens disclosed a squamous cell carcinoma with Hassall's corpuscle-like keratotic pearls, and an immunohistological study showed a positive staining with PTHrP. The tumor and serum PTHrP concentration markedly decreased following cisplatin-based chemotherapy and radiation. This is the first case of PTHrP producing a thymic carcinoma with the unusual presentation of a large extrathoracic mass.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

Parathyroid and thyroid function five years after treatment of laryngeal and hypopharyngeal carcinoma.

The proximity of the thyroid and parathyroid glands to the larynx and hypopharynx puts them at risk from treatment of squamous cell carcinoma (SCC) of this region. Consequently parathyroid and thyroid function was evaluated in patients surviving at least 5 years following treatment of primary SCC of the larynx or hypopharynx. Twenty-eight patients, initially treated from 1990 to 1992, were assessed and divided into four groups according to treatment received. Hypoparathyroidism (partial and hypocalcaemic) occurred in 88% and hypothyroidism (clinical and subclinical) in 50% in Group 1 (radiotherapy only) Group 2 (salvage laryngectomy for failed radiotherapy) had 66% hypoparathyroid and 33% hypothyroid. Group 3 (surgery + radiotherapy combined) had 89% hypoparathyroid and 89% hypothyroid. Group 4 (surgery only) had 63% hypoparathyroid and 63% hypothyroid. Significant endocrine hypofunction therefore occurs following the treatment of laryngopharyngeal carcinoma, more so with radiotherapy and combined therapy than with surgery alone.

Carcinoma, Squamous Cell↗
PubMed1991

Locally recurrent parathyroid neoplasms as a cause for recurrent and persistent primary hyperparathyroidism.

Between 1982 and 1989, 145 patients underwent operations for persistent or recurrent primary hyperparathyroidism (HPT). At re-exploration, 15 patients (10.3%) were found to have locally recurrent parathyroid tumors (11 patients with adenoma and 4 with carcinoma). These 15 patients had 28 previous operations at outside institutions for HPT. Patients with locally recurrent HPT secondary to adenoma had a longer disease-free interval than patients with locally recurrent carcinoma. At the time of evaluation at the National Institutes of Health (NIH) for recurrent or persistent HPT, each patient was symptomatic and patients with carcinoma had significantly more symptoms and higher serum levels of calcium and parathyroid hormone than patients with adenoma. Locally recurrent parathyroid neoplasm was correctly localized by preoperative testing in 14 of 15 patients. These 15 patients underwent 18 reoperations at NIH for excision of locally recurrent parathyroid tumors. Following the final reoperation (two patients had more than one procedure), each patient had normal serum levels of calcium. In addition each patient remains biochemically cured (based on normal serum calcium level), with a median follow-up interval of 21 months. Local recurrence of parathyroid adenoma comprises a small but significant proportion of cases of recurrent or persistent HPT and can be indistinguishable from parathyroid carcinoma. Findings suggestive of carcinoma include shorter disease-free interval, higher serum levels of calcium and parathyroid hormone, and histologic appearance. Whether the locally recurrent parathyroid neoplasm is benign or malignant, aggressive surgery can control serum levels of calcium in these patients with acceptable rates of morbidity.

Adenoma↗
PubMed1998

Regulation of parathyroid hormone-related protein expression in MCF-7 breast carcinoma cells by estrogen and antiestrogens.

Expression of parathyroid hormone-related protein (PTHrP) in breast carcinoma is a frequent cause of the paraneoplastic syndrome of hypercalcemia. In response to treatment with estrogen or tamoxifen, some breast cancer patients also develop a transient hypercalcemia. Therefore, the effect of 17beta-estradiol (E2), tamoxifen, or its more potent metabolite, 4-hydroxytamoxifen (OH-tamoxifen), on PTHrP expression in an estrogen receptor (ER)-positive breast carcinoma cell line (MCF-7) was evaluated. E2 increased PTHrP mRNA levels in MCF-7 cells and stimulated PTHrP(1-86) release in a dose-dependent fashion (10(-10)-10(-6) M). Tamoxifen and OH-tamoxifen also stimulated PTHrP release in a concentration-dependent fashion that paralleled their relative ER binding affinities (10(-6) or 10(-8)-10(-6) M, respectively). Combined treatment with the partial estrogen agonist, OH-tamoxifen, and E2 decreased E2-stimulated PTHrP secretion in MCF-7 cells to the levels seen with OH-tamoxifen treatment alone. These results suggest that transient estrogen- or tamoxifen-induced hypercalcemia in patients with breast carcinoma may be a PTHrP-mediated effect that is a marker of ER positivity.

Breast Neoplasms↗