Animal model of Pancreatic Cancer

我们建立了LSL- kras G12D（条件K-ras突变体）、LSL p53 R172 H（条件p53突变体）、Pdx-1-Cre（胰腺特异性cre重组酶转基因）、NOS2-和IL-6缺陷小鼠的菌落。我们也培育了nos2缺陷的LSL-Kras G12D小鼠。为了激活条件突变的K-ras和p53等位基因，这些小鼠与Pdx-1-Cre小鼠杂交。将IL-6缺陷小鼠与LSL-Kras G12D（条件K-ras突变体）杂交，生成IL-6缺陷条件K-ras突变体小鼠。在激活Kras和p53双突变小鼠后，超过90%的小鼠在3-6个月内发生PDAC。这些小鼠将与缺乏NOS2或IL-6或使用抗mif抗体治疗的Kras和p53双突变小鼠进行比较。

We have established the colonies of LSL-Kras G12D (conditional K-ras mutant), LSL p53 R172 H (conditional p53 mutant), Pdx-1-Cre (pancreas-specific Cre-recombinase transgenic), NOS2- and IL-6 -deficient mice. We have also generated NOS2-deficient LSL-Kras G12D mice. To activate the conditional mutant K-ras and p53 alleles these mice are being bred with Pdx-1-Cre mice. IL-6 deficient mice are crossed with LSL-Kras G12D (conditional K-ras mutant) to generate IL-6-deficient conditional K-ras mutant mice. Following activation, the Kras and p53 double mutant mice will develop PDAC in 3-6 months in more than 90% of mice. These mice will be compared with those Kras and p53 double mutant mice that lack either NOS2 or IL-6 or are treated with anti-MIF antibody.