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Cancer Types / Endocrine System Cancers / Parathyroid Cancer / NCI Resources

NCI CANCERLIT^® Search: Parathyroid Cancer - June 2002

National Cancer Institute^®
Last Modified: June 1, 2002

Painful ophthalmoplegia from metastatic nonproducing parathyroid carcinoma: case study and review of the literature.
Severe osteoporosis and autonomous hyperparathyroidism: making the numbers add up.
[On the isotopic localization of parathyroid adenomas]
Brown tumor of the sternum.
Mitogen-activated protein kinase cascade in human normal and tumoral parathyroid cells.
Marked uptake of technetium-99m pertechnetate by parathyroid adenoma.
Genetic analysis of lithium-associated parathyroid tumors.
[A case of secondary hyperparathyroidism with an ectopic intrathyroid gland successfully diagnosed and controlled by percutaneous ethanol

Table of Contents

1
UI - 11772432
AU - Eurelings M; Frijns CJ; Jeurissen FJ
TI - Painful ophthalmoplegia from metastatic nonproducing parathyroid carcinoma: case study and review of the literature.
SO - Neuro-oncol 2002 Jan;4(1):44-8
AD - Department of Neurology, University Medical Center, Utrecht, The Netherlands.
Parathyroid carcinoma is an uncommon malignancy. Of the fewer than 400 cases reported, most have been cases of producing parathyroid carcinoma with accompanying hypercalcemia. Only 13 patients with nonproducing parathyroid carcinoma have been described. Nine of these 13 patients had metastatic disease. We report a patient with i.c. metastasis. Distal metastases of producing parathyroid carcinoma are treated surgically to prolong survival and prevent complications of hyperparathyroidism and hypercalcemia. One half of the patients with producing parathyroid carcinoma die within 5 years, mostly because of the complications of hypercalcemia. Nonproducing parathyroid carcinoma compares unfavorably with producing parathyroid carcinoma in terms of tumor progression and prognosis. Few data on choice of therapy in nonproducing parathyroid carcinoma are available. We treated our patient with a combination of radiotherapy and chemotherapy. Treatment was followed by an unexpectedly prolonged survival of 31 months after diagnosis of metastatic disease.

2
UI - 11937656
AU - Weis U; Meeking DR; Cummings MH
TI - Severe osteoporosis and autonomous hyperparathyroidism: making the numbers add up.
SO - QJM 2002 Apr;95(4):255-7

3
UI - 11879624
AU - Garcia Perez I; Pozo Fidalgo F; Ricarte Perez P; Garcia-Moran M
TI - [On the isotopic localization of parathyroid adenomas]
SO - Rev Esp Med Nucl 2002 Apr;21(2):126-7
AD - Servicio de Cirugia General II, Hospital Central de Asturias, Spain.

4
UI - 12022577
AU - Kao CL; Chang JP; Lin JW; Lin CC
TI - Brown tumor of the sternum.
SO - Ann Thorac Surg 2002 May;73(5):1651-3
AD - Department of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital at Kaohsiung, Kaohsiung Hsien, Taiwan, Republic of China. sa11421@adm.cgmh.org.tw
The skeletal changes of severe hyperparathyroidism, known as osteitis fibrosa cystica, are now rarely encountered, because hyperparathyroidism is currently being diagnosed and treated at an early stage. Herein, a case of brown tumor of the sternum is reported; our report adds histologic data on this type of tumor to the literature.

5
UI - 11994364
AU - Corbetta S; Lania A; Filopanti M; Vicentini L; Ballare E; Spada A
TI - Mitogen-activated protein kinase cascade in human normal and tumoral parathyroid cells.
SO - J Clin Endocrinol Metab 2002 May;87(5):2201-5
AD - Institute of Endocrine Science, Ospedale Maggiore IRCCS, Milan, Italy 20122.
The calcium-sensing receptor (CaR) activation has recently been shown to modulate the ERK1 and ERK2 cascade in different cell lines. The present study investigated this pathway in human normal and tumoral parathyroid cells. In cells from normal parathyroids and almost all hyperplasia increasing extracellular calcium concentrations (Ca(o)(2+)) induced a significant activation of ERK1 and -2, the percent stimulation over basal activity (at 0.5 mM Ca(o)(2+)) being 545 +/- 140 and 800 +/- 205 in normal cells and 290 +/- 71 and 350 +/- 73 in hyperplasia at 1 and 2 mM Ca(o)(2+), respectively. This effect was mediated by CaR because it was mimicked by the receptor agonist gadolinium and neomycin. Basal and Ca(o)(2+)-stimulated ERK1 and -2 activity was nearly abolished by the PKC inhibitor calphostin C, and PKA changes did not affect ERK1 and -2 activity. PI3K blockade by wortmannin, known to prevent G protein betagamma subunit effect on ERK1 and -2, induced a 30% reduction of the Ca(o)(2+)-stimulated ERK1 and -2 activity. Adenomatous cells showed high PKC-dependent ERK1 and -2 activity in resting conditions that was unresponsive to high Ca(o)(2+). A role of MAPK on PTH secretion was suggested by the finding that PD98059, a specific MEK inhibitor, abolished the inhibitory effect of 1.5 mM Ca(o)(2+) on PTH release from normal parathyroid cells. In conclusion, these data first demonstrate that CaR activation, through the PKC pathway and, to a lesser extent, PI3K, increases ERK1 and -2 activity in normal parathyroid cells and this cascade seems to be involved in the modulation of PTH secretion by Ca(o)(2+). Interestingly, this signaling pathway is disrupted in parathyroid tumors.

6
UI - 11446675
AU - Kikuchi T; Watanobe H; Suda T; Tomiyama T; Masuda M
TI - Marked uptake of technetium-99m pertechnetate by parathyroid adenoma.
SO - Intern Med 2001 Jun;40(6):506-9
AD - First Department of Internal Medicine, Aomori City Hospital, Katta.
We herewith report an unusual case of primary hyperparathyroidism whose parathyroid adenoma strongly accumulated technetium (Tc)-99m pertechnetate. A 41-year-old woman was referred to our department under the tentative diagnosis of primary hyperparathyroidism. Scintigraphy by thallium-201 chloride showed homogeneous uptake in the whole thyroid, whereas Tc-99m image revealed a strong local accumulation in the middle portion of the right thyroidal lobe. Neck exploration revealed a 12x8x5 mm tumor in the posterolateral region of the right thyroidal lobe, the pathology of which was parathyroid adenoma. In addition, a small nodule (8 mm in diameter) with pathological findings revealing follicular adenoma of the thyroid, was found within the medial portion of the right thyroidal lobe. Both lesions were removed by surgery, and a postoperative Tc-99m scintigraphy no longer demonstrated a significant uptake in the right thyroidal lobe. Since the thyroid adenoma was too small to be detected by any scintigraphic study and located much closer to the median line than the site of the marked accumulation of Tc-99m pertechnetate, it was considered very likely that the parathyroid adenoma concentrated Tc-99m. Search of literature revealed that there have been only thirteen cases of parathyroid tumor reported to date which significantly accumulated Tc-99m pertechnetate. The present patient represents another rare case of parathyroid adenoma showing sueh an unusual scintigraphic image.

7
UI - 11980616
AU - Dwight T; Kytola S; Teh BT; Theodosopoulos G; Richardson AL; Philips J;
TI - Twigg S; Delbridge L; Marsh DJ; Nelson AE; Larsson C; Robinson BG Genetic analysis of lithium-associated parathyroid tumors.
SO - Eur J Endocrinol 2002 May;146(5):619-27
AD - Cancer Genetics Unit, Kolling Institute of Medical Research, Royal North Shore Hospital, Sydney, Australia.
OBJECTIVE: The aim of this study was to determine the primary genetic events that may underlie the formation of parathyroid tumors in patients with lithium-associated hyperparathyroidism (HPT). METHODS: Comparative genomic hybridization (CGH), loss of heterozygosity (LOH) and multiple endocrine neoplasia type 1 gene (MEN1) mutation analysis were used to analyze twelve parathyroid tumors from nine patients with lithium-associated HPT. For comparison, CGH was also carried out in a non-lithium-associated group of thirteen sporadic parathyroid tumors. RESULTS: A higher prevalence of multiglandular disease in the lithium-associated HPT patients compared with the idiopathic sporadic patients was observed (Fisher's exact test, P=0.02). CGH alterations were detected in four lithium-associated parathyroid tumors, involving loss at 1p, 11, 15q, 22q and gain of the X chromosome. In addition, one of these four cases exhibited LOH at 11q13 and was found to contain a novel somatic MEN1 mutation (c.1193insTAC). Although fewer lithium-associated parathyroid tumors were shown to contain genetic alterations compared with the sporadic parathyroid tumors, the changes detected were those frequently associated with both familial and sporadic parathyroid tumorigenesis. CONCLUSION: This is, to our knowledge, the first genetic analysis of parathyroid tumors in lithium-associated HPT patients. Our data indicated that the majority of lithium-associated parathyroid tumors do not contain gross chromosomal alterations and suggest that in most cases the tumorigenic pathway is independent of MEN1 and genes at 1p34.3-pter and 1q21-q32. It is possible that other discrete genetic alterations or epigenetic changes, not screened for in this study, could also be responsible for parathyroid tumorigenesis in lithium-associated HPT.

8
UI - 12073627
AU - Tanaka M; Itoh K; Matsushita K; Ogawa A; Hirayama H; Tsunoda N;
TI - Yoshizumi K; Naruse M; Nonoguchi H; Tomita K [A case of secondary hyperparathyroidism with an ectopic intrathyroid gland successfully diagnosed and controlled by percutaneous ethanol injection therapy (PEIT)]
SO - Nippon Jinzo Gakkai Shi 2002 May;44(4):409-13
AD - NTT Nishinippon Kyushu General Hospital, Japan.
Secondary hyperparathyroidism (II HPT) is a major complication in chronic dialysis patients, and percutaneous ethanol injection therapy (PEIT) has become a useful alternative treatment for II HPT. However, the existence of ectopic parathyroid glands is a major problem when conducting PEIT. Ectopic parathyroid gland accepts 10-35% of II HPT, and the missing glands cannot be detected consistently by any imaging techniques, including scintigraphy. Intrathyroid parathyroid gland is as rare as about 1% and recurrence of missing glands after parathyroidectomy (PTx) has been reported in some cases. We report here a 52-year-old female in whom an ectopic parathyroid gland was defected successfully and intact-PTH controlled by tentative PEIT. At the first examination, a left parathyroid adenoma and a right thyroid goiter were pointed out by ultrasonography, CT and scintigraphy. PEIT was applied twice to the left parathyroid adenoma, but intact-PTH was not decreased. Ultrasonography, CT, 201Tl-99mTc subtraction scintigraphy and fine needle aspiration biopsy (FNAB) were performed again to search for the existence of ectopic glands. The results suggested that the right intrathyroid tumor was an ectopic parathyroid gland. Consequently, tentative PEIT was applied to the right intrathyroid tumor, and successful control of intact-PTH and serum Ca was eventually achieved. To our knowledge, this is the first reported case of secondary hyperparathyroidism with an ectopic intrathyroid gland that was successfully controlled by PEIT. In this case, it was suggested that tentative PEIT of intrathyroid tumor was a useful method for detecting an ectopic parathyroid gland.

The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.

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