KC 和 KPC 胰腺导管腺癌小鼠模型在建模生物学及其临床相关性方面的差异。
Differences between KC and KPC pancreatic ductal adenocarcinoma mice models, in terms of their modeling biology and their clinical relevance.
机构信息
Department of Clinical Laboratory, The Second Hospital of Shandong University, 247 Beiyuan Street, Jinan, 250033, Shandong, China.
Department of Clinical Laboratory, The Second Hospital of Shandong University, 247 Beiyuan Street, Jinan, 250033, Shandong, China; International Biotechnology R&D Center, Shandong University School of Ocean, 180 Wenhua Xi Road, Weihai, Shandong, 264209, China.
出版信息
Pancreatology. 2020 Jan;20(1):79-88. doi: 10.1016/j.pan.2019.11.006. Epub 2019 Nov 18.
Pancreatic ductal adenocarcinoma (PDAC) is among the dangerous human cancers, is the 10th highly prevalent cancer, and the fourth sole cause of cancer-related mortality in the United States of America. Notwithstanding the significant commitment, the forecast for people with this burden continues to have a five-year survival rate of just 4-6%. The most critical altered genes within PDAC consist of K-ras the proto-oncogene which is usually mutationally activated above 90% cases and tumor suppressors likeTrp53 are altered at 55%. To face the burden of pancreatic ductal adenocarcinoma, a variety of genetically engineered pancreatic cancer mice models have been created over the last past years. These models have distinctive features and are not all appropriate for preclinical studies. In this review, we focus on differences between two mice models K-ras;Pdx-1-Cre(KC) and K-ras; Trp53; Pdx-1-Cre(KPC) in terms of their modeling biology and their clinical relevance.
胰腺导管腺癌（PDAC）是一种危险的人类癌症，是第 10 种高发癌症，也是美国癌症相关死亡的第四大单一原因。尽管做出了巨大的努力，但这种疾病的患者的预后仍然只有 5 年生存率为 4-6%。PDAC 中最关键的改变基因包括原癌基因 K-ras，其在超过 90%的病例中通常发生突变激活，而肿瘤抑制基因如 Trp53 在 55%的病例中发生改变。为了应对胰腺导管腺癌的负担，过去几年已经创建了多种基因工程胰腺癌细胞模型。这些模型具有不同的特点，并非都适合临床前研究。在这篇综述中，我们专注于 K-ras 基因两种小鼠模型（KC 和 KPC）之间在建模生物学和临床相关性方面的差异。
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