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首页> 外文期刊>Molecular and Cellular Biology >Of Mice and MEN1: Insulinomas in a Conditional Mouse Knockout
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Of Mice and MEN1: Insulinomas in a Conditional Mouse Knockout

机译：小鼠和MEN1：条件性小鼠基因敲除中的胰岛素瘤

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Patients with multiple endocrine neoplasia type 1 (MEN1) develop multiple endocrine tumors, primarily affecting the parathyroid, pituitary, and endocrine pancreas, due to the inactivation of the MEN1 gene. A conditional mouse model was developed to evaluate the loss of the mouse homolog, Men1, in the pancreatic beta cell. Men1 in these mice contains exons 3 to 8 flanked by loxP sites, such that, when the mice are crossed to transgenic mice expressing cre from the rat insulin promoter (RIP-cre), exons 3 to 8 are deleted in beta cells. By 60 weeks of age, >80% of mice homozygous for the floxed Men1 gene and expressing RIP-cre develop multiple pancreatic islet adenomas. The formation of adenomas results in elevated serum insulin levels and decreased blood glucose levels. The delay in tumor appearance, even with early loss of both copies of Men1, implies that additional somatic events are required for adenoma formation in beta cells. Comparative genomic hybridization of beta cell tumor DNA from these mice reveals duplication of chromosome 11, potentially revealing regions of interest with respect to tumorigenesis.
机译：多发性内分泌肿瘤1型（MEN1）的患者会发展多发性内分泌肿瘤，这主要是由于 MEN1 基因的失活，主要影响甲状旁腺，垂体和内分泌胰腺。建立了条件小鼠模型来评估胰腺β细胞中小鼠同源物 Men1 的丢失。这些小鼠中的 Men1 包含侧翼为loxP位点的外显子3至8，因此，当小鼠与表达来自大鼠胰岛素启动子的cre的转基因小鼠（RIP-cre）杂交时，外显子3至8是在beta细胞中删除。到60周龄时，> 80％的小鼠对 Men1 信号的表达是纯合的，并且表达RIP-cre会发展出多个胰岛腺瘤。腺瘤的形成导致血清胰岛素水平升高和血糖水平降低。即使 Men1 的两个拷贝都早丢失，肿瘤出现的延迟也意味着β细胞中腺瘤形成需要额外的体细胞事件。来自这些小鼠的β细胞肿瘤DNA的比较基因组杂交揭示了11号染色体的重复，潜在地揭示了关于肿瘤发生的感兴趣区域。

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