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Endocrine tumor thyroid tumors

Ectopic ACTH syndrome refers to excessive ACTH production resulting from an endocrine or nonendocrine tumor, usually of the pancreas, thyroid, or lung (e.g., small-cell lung cancer). [Pg.216]

Enolase is a glycolytic enzyme also known as phosphopyru-vate hydratase. Neuron-specific enolase (NSE) is the form of enolase found in neuronal tissue and in the cells of the diffuse neuroendocrine system and the amine precursor uptake, and decarboxylation (APUD) tissue. NSE is found in tumors associated with the neuroendocrine origin, including small cell lung cancer (SCLC), neuroblastoma, pheochromocytoma, carcinoid, medullary carcinoma of the thyroid, melanoma, and pancreatic endocrine tumors. [Pg.756]

Cai YC, Banner B, Glickman J, Odze RD. Cytokeratin 7 and 20 and thyroid transcription factor-1 can help distinguish pulmonary from gastrointestinal carcinoid and pancreatic endocrine tumors. Hum Pathol. 2001 32 1087-1093. [Pg.337]

Mazzaferri, E.L. (1993). Thyroid carcinoma papillary and follicular. In (eds E.L. Mazzaferri and N. Samaan), Endocrine Tumors. Blackwell Scientific, Cambridge, MA. [Pg.1022]

Tumorigenic - Carcinogenic by RTECS criteria Endocrine - thyroid tumors Mutation in mammalian somatic cells (mouse lymphocyte) = 1500 mg/L... [Pg.45]

Several lines of evidence indicate that macromolecules of as yet unidentified chemical nature, produced by cancers and released into the systemic circulation, are responsible for the biochemical alterations in the liver and other host organs. In view of the diverse regulatory properties of the many different enzymes that increase or decrease towards their immature level (see Table III), a deficiency or excess in any given endocrine or dietary factor can clearly not explain the phenomenon. Nor has it been possible to implicate reductions in the efficacy of these factors. Subnormal concentration of the nuclear thyroid hormone receptor has been noted in the liver of tumor-bearing animals(24) however, since losses in the T3-inducible catalysts of the same liver occurred at much earlier stages of tumor-bearing,(24) the subnormal receptor concentration could clearly not be the cause of these losses but was probably another, and rather late, reflection of the process of biochemical undifferentiation. [Pg.355]

Calcitonin is secreted by the parafollicular or C cells, which arise from the neural crest and are distributed throughout the thyroid gland. These cells are included in the APUD (cmine precursor uptake and decarboxylation) family, which explains the association of medullary thyroid carcinoma (a tumor of the C cells) and other tumors of the APUD family in multiple endocrine neoplasia type 2A and -2B (MEN-2A and MEN-2B). Release of calcitonin is stimulated by calcium, and it has been used pharmacologically as an inhibitor of bone resorption. [Pg.1926]

Poorly differentiated endocrine neoplasms, depending on the site of origin, may produce characteristic peptide hormones. The group of poorly differentiated neuroendocrine tumors and their hormone production include islet cell tumors (insulin, glucagon, somatostatin, gastrin), pulmonary small cell carcinoma (bombesin in 45% of cases), and medullary thyroid carcinoma (calcitonin). [Pg.226]

Weber F, Aldred MA, Morrison C, Plass C, Frilling A, Broelsch CE, Waite K, Eng C. Silencing of the maternally imprinted tumor suppressor ARHI contributes to follicular thyroid carcinogenesis. J Clin Endocrin Metabol. 2005 90 1149-55. [Pg.725]


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