Molecular mechanisms of primary hyperparathyroidism.
Several advances have been achieved toward the goal of understanding the molecular basis of parathyroid tumorigenesis. The cyclin D1/PRAD1 oncogene has been identified, and is involved in the development of several different tumor types besides those of the parathyroid. The tumor suppressor RB gene has been linked to the pathogenesis of parathyroid carcinoma. The MEN-1 gene product has been identified and mutations in MENIN shown to contribute to sporadic tumors. An understanding of the functions of MENIN will provide further insights into parathyroid disease. Mutations in the RET gene have been identified as the causal agent in MEN-2 but this gene contributes rarely to development of sporadic parathyroid tumors. Ultimately, a description of parathyroid tumorigenesis will need to account for such features as the rarity of parathyroid carcinoma, the increased incidence of tumors after neck irradiation, and the increased frequency of hyperparathyroidism in postmenopausal women. In addition, the relationship between excessive cellular proliferation and an altered set-point in the mechanism linking extracellular calcium concentration to PTH secretion requires explanation. While mutations in the CASR gene itself play a critical role in familial disease, they do not appear to be involved in sporadic parathyroid tumorigenesis, and investigation of genes important for its expression is clearly warranted.[1]References
- Molecular mechanisms of primary hyperparathyroidism. Hendy, G.N. Reviews in endocrine & metabolic disorders. (2000) [Pubmed]
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