parathyroid neoplasms/tyrosine

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18F-Fluorocholine, 18F-FDG, and 18F-Fluoroethyl Tyrosine PET/CT in Parathyroid Cancer.

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We report on a 71-year-old woman presenting with biochemical features indicating recurrent disease in long-term follow-up of left-sided parathyroid carcinoma. She had undergone several surgical procedures including total thyroidectomy, partial resection of the esophageal wall, and curative neck

Obvious mRNA and protein expression but absence of mutations of the RET proto-oncogene in parathyroid tumors.

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The study on the expression of the RET proto-oncogene in parathyroid tumors disclosed obvious mRNA expression by the reverse transcription (RT)-polymerase chain reaction (PCR) method and protein expression by Western blotting. To find out whether mutations in the cysteine-rich regions or tyrosine

Genetics of parathyroid tumours.

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Primary hyperparathyroidism (PHPT), due to parathyroid tumours, may occur as part of a complex syndrome or as an isolated (nonsyndromic) disorder, and both forms can occur as familial (i.e. hereditary) or nonfamilial (i.e. sporadic) disease. Syndromic PHPT includes multiple endocrine neoplasia (MEN)

Identification of a novel activated form of the keratinocyte growth factor receptor by expression cloning from parathyroid adenoma tissue.

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Parathyroid adenomas are benign tumors in the parathyroid glands, whose pathogenesis is largely unknown. We utilized an expression cDNA cloning strategy to identify oncogenes activated in parathyroid adenomas. An expression cDNA library was prepared directly from a clinical sample of parathyroid

Immunohistochemical investigation of angiogenic factors in parathyroid proliferative lesions.

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OBJECTIVE The pathological distinction between parathyroid neoplasms and hyperplasias remains difficult in several cases. Endoglin (CD105) is a proliferation-associated and hypoxia-inducible protein abundantly expressed in angiogenic endothelial cells. Vascular endothelial growth factor (VEGF)

Genetic testing in multiple endocrine neoplasia and related syndromes.

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Multiple Endocrine Neoplasia (MEN) syndromes are inherited diseases characterised by endocrine tumours occuring as autosomal dominant genetic diseases with high penetrance. In MEN1, most tumours affect the parathyroids, endocrine pancreas, anterior pituitary, and adrenal glands. The MEN1 gene has

Differential expression of microRNAs in human parathyroid carcinomas compared with normal parathyroid tissue.

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Parathyroid carcinoma (PaC) is a rare cause of primary hyperparathyroidism. Though the loss of the oncosuppressor CDC73/HRPT2 gene product, parafibromin, has been involved in the hyperparathyroidism-jaw tumor syndrome and in a consistent set of sporadic PaCs, parathyroid carcinogenesis remains

Genetic analysis and clinical investigation of a pedigree with multiple endocrine neoplasia type 2A: A case report.

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Multiple endocrine neoplasia 2A (MEN2A) is characterized by the coexistence of tumors that involve two or more endocrine glands within the same patient, and is defined as the occurrence of medullary thyroid carcinoma in association with pheochromocytoma (PHEO) and parathyroid tumors or

Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4).

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Multiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2

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