原发性甲状旁腺功能亢进
甲状旁腺腺瘤
内科学
甲状旁腺激素
医学
多发性内分泌肿瘤
钙敏感受体
内分泌学
甲状旁腺癌
腺瘤
甲状旁腺主细胞
甲状旁腺肿瘤
继发性甲状旁腺功能亢进
作者
Steven K. Libutti,Judy S. Crabtree,Dominique Lorang,A. Lee Burns,C.M. Mazzanti,Stephen M. Hewitt,Sarah O'Connor,Jerrold M. Ward,Michael R. Emmert-Buck,Alan T. Remaley,Marshall Miller,Ewa M. Turner,H. Richard Alexander,Andrew Arnold,Stephen J. Marx,Francis S. Collins,Allen M. Spiegel
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2003-11-15
卷期号:63 (22): 8022-8028
被引量:86
摘要
The inactivation of the MEN1 tumor suppressor gene in patients leads to a constellation of changes in endocrine tissues, including parathyroid neoplasia, pituitary adenomas, pancreatic neuroendocrine tumors, and carcinoids. To study the pathophysiological consequences of the deletion of the MEN1 gene, we set out to create a mouse model of hyperparathyroidism resulting from the deletion of the Men1 gene in parathyroid tissue. We introduced a Men1 gene flanked by loxP sites into the mouse germ line and then used a parathyroid cell-specific promoter to drive the expression of Cre recombinase, resulting in the deletion of the Men1 gene. Here, we show that loss of Men1 gene function in the parathyroid glands of mice results in histological changes consistent with parathyroid neoplasia as well as systemic hypercalcemia. This model provides a means for dissecting the molecular basis of this familial cancer syndrome and may allow for the development of new strategies to treat related forms of hypercalcemia.
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