Targeting tumor microenvironment as a novel therapeutic strategy for pancreatic cancer using a genetically-engineered mouse model

一种基因工程小鼠模型，包含突变Kras表达和Tgfbr2敲除，概括了人类胰腺癌的组织学特征，显示腺癌具有丰富的纤维化。小鼠胰腺癌细胞分泌CXCR2配体，诱导间质成纤维细胞表达CTGF，通过血管生成促进肿瘤。抑制肿瘤微环境中肿瘤-基质相互作用显示出抗肿瘤作用，可作为胰腺癌的一种治疗选择。胰腺癌组织中含有丰富的巨噬细胞浸润，然而，靶向巨噬细胞作为胰腺癌的治疗方法还有待进一步研究。

A genetically-engineered mouse model, containing mutant Kras expression and Tgfbr2 knockout, recapitulates histological features of human pancreatic cancer, demonstrating adenocarcinoma with abundant fibrosis. The murine pancreatic cancer cells secret CXCR2 ligands, which induce CTGF expression in the stromal fibroblasts, resulting in tumor promotion through angiogenesis. Inhibiting the tumor-stromal interactions in the tumor microenvironment demonstrated anti-tumor effect and can be a therapeutic option for pancreatic cancer. The pancreatic cancer tissues contain abundant macrophage infiltration, however, targeting the macrophages as a therapy of pancreatic cancer should be further investigated.