| Autor: |
G V, Walls, M, Stevenson, K E, Lines, P J, Newey, A A C, Reed, M R, Bowl, J, Jeyabalan, B, Harding, K J, Bradley, S, Manek, J, Chen, P, Wang, B O, Williams, B T, Teh, R V, Thakker |
| Rok vydání: |
2016 |
| Předmět: |
|
| Zdroj: |
Oncogene |
| ISSN: |
1476-5594 |
| Popis: |
The hyperparathyroidism-jaw tumour (HPT-JT) syndrome is an autosomal dominant disorder characterized by occurrence of parathyroid tumours, often atypical adenomas and carcinomas, ossifying jaw fibromas, renal tumours and uterine benign and malignant neoplasms. HPT-JT is caused by mutations of the cell division cycle 73 (CDC73) gene, located on chromosome 1q31.2 and encodes a 531 amino acid protein, parafibromin. To facilitate in vivo studies of Cdc73 in tumourigenesis we generated conventional (Cdc73+/−) and conditional parathyroid-specific (Cdc73+/L/PTH-Cre and Cdc73L/L/PTH-Cre) mouse models. Mice were aged to 18-21 months and studied for survival, tumour development and proliferation, and serum biochemistry, and compared to age-matched wild-type (Cdc73+/+ and Cdc73+/+/PTH-Cre) littermates. Survival of Cdc73+/− mice, when compared to Cdc73+/+ mice was reduced (Cdc73+/−=80% Cdc73+/+=90% at 18 months of age, Pfourfold higher than that in parathyroid glands of wild-type littermates (P |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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