Animal model of Pancreatic Cancer

我们已经建立了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缺陷小鼠的克隆。我们还产生了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小鼠交配。将IL-6缺陷小鼠与LSL-Kras G12D(条件性K-ras突变体)杂交，产生IL-6缺陷的条件性K-ras突变小鼠。激活后，Kras和P53双突变小鼠将在3-6个月内在90%以上的小鼠中发生PDAC。这些小鼠将与那些缺乏NOS2或IL-6或接受抗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.