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中文摘要
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我们建立了LSL-Kras G12 D(条件性K-ras突变体)、LSL p53 R172 H(条件性p53突变体)、Pdx-1-Cre(胰腺特异性Cre重组酶转基因)和NOS 2、IL-6和MIF基因敲除小鼠的集落。LSL-Kras G12 D、p53 R172 H和Pdx-1-Cre的杂交产生了三重突变小鼠,其发展为PDAC,中位存活期约为5个月,到12个月时死亡率几乎为100%。通过将这些品系与NOS 2缺陷小鼠杂交,我们建立了NOS 2缺陷胰腺癌小鼠模型。这些小鼠代表不同的遗传组合的七组已经成立,以研究一氧化氮在胰腺导管腺癌的发展和进展中的作用。类似的策略被用于产生MIF和IL-6缺陷的胰腺癌小鼠模型。
英文摘要
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), and NOS2-, IL-6- and MIF-knockout mice. Inter-breeding of LSL-Kras G12D, p53 R172 H and Pdx-1-Cre generates the triple mutant mice that develop PDAC with a median survival of approximately 5 months and almost 100% mortality by 12 months. By cross-breeding these strains with NOS2 deficient mice, we have generated NOS2-deficient pancreatic cancer mouse model. Seven groups of these mice representing different genetic combinations have been set up to investigate the role of nitric oxide in the development and progression of pancreatic ductal adenocarcinoma. Similar strategy is being used to generate MIF- and IL-6 deficient pancreatic cancer mouse models.
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Role of Immune and Inflammation Mediators in Progression of Pancreatic Cancer
Forkhead-box (FOX) Transcription Factors in the Progression of Pancreatic Cancer
Integrative Molecular Profiling of Human Pancreatic Cancer
Molecular Profiling of Pancreatic Cancer
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