Analysis of the new joint protein receptor of PSTI

我们的目的是研究假设胰腺癌的治疗策略和阐明新的PST受体。关于一种新的受体，除了EGFR外，我们无法确定一种有效的受体。因此，我们利用基因改变技术控制PSTI基因表达，建立两种发病机制的慢性胰腺炎模型小鼠，检测与胰腺纤维化有关的胰腺星状细胞、Krasgene、EGFR家族基因的激活、INK4a基因的表达。ki67阳性腺泡细胞异常增多，形成管状结构。Kras基因（EGFR家族基因）的表达在慢性胰腺炎中已经存在，这表明它是向癌前病变的过渡阶段。

We aimed for the treatment strategy which assumed pancreatic cancer and elucidation ofa new receptor with PST. About a new receptor, we were not able to identify an effectivereceptor except EGFR. So, we established chronic pancreatitis model mouse of two kindsof onset mechanism by controlling PSTI gene expression using gene change technology andexamined activation of a pancreas stellate cell concerned with pancreatic fibrosis, Krasgene, EGFR family gene, expression of INK4a gene. We showed an abnormal increase withKi67 positive acini cell which formed duct -like structure. Expression of a Kras gene,an EGFR family gene was already present in conditions of chronic pancreatitis, and itwas suggested that it was a transition stage to precancerosis.