CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer. CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer
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https://www.ncbi.nlm.nih.gov/bioproject/PRJNA781603
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资源简介:
Kras and Trp53 mutations promote transformation in pancreatic acinar and ductal cells. We wanted to evaluate whole transcriptomic profiles of acinar and ductal derived tumors. In addition, we studied whole transcriptomic changes in ex vivo cultured ducts expressing mutant Kras compared to control ducts. Overall design: Mutant Kras and mutant Trp53 were genetically deleted from acinar or ductal cells using inducible CRE:ER alleles. Eight week old mice were given tamoxifen (5mg) in corn oil and mice were monitored for signs of disease progression.
KRAS(Kras)与TP53(Trp53)突变可促进胰腺腺泡细胞与导管细胞的恶性转化。本研究旨在评估腺泡细胞及导管细胞来源肿瘤的全转录组表达谱。此外,本研究还对比分析了表达突变KRAS(Kras)的体外(ex vivo)培养导管与对照导管的全转录组变化。实验设计概况:本研究通过诱导型CRE:ER等位基因,从腺泡细胞或导管细胞中敲除突变型KRAS(Kras)与突变型TP53(Trp53)。向8周龄小鼠给予玉米油配制的他莫昔芬(tamoxifen,5mg),并持续监测小鼠的疾病进展征象。
创建时间:
2021-11-18



