胰腺癌恶性程度高、预后极差。当前胰腺癌的生物医学基础研究，已从侧重于研究肿瘤细胞自身的生物学行为及其调控机理，深入发展到对肿瘤微环境的改变，及其改变对肿瘤细胞恶性生物学行为的影响研究。肿瘤相关巨噬细胞（TAM）是胰腺癌免疫微环境的重要组成部分。近期文献报道和本课题组工作发现，胰腺癌细胞在一定微环境条件下可诱导TAM呈现出不同的表型和功能。但胰腺癌细胞和TAM相互作用的途径和机制尚不明确。最新研究发现，不同生物种类的细胞中可产生一种新的胞外细胞器—迁移体，迁移体可能参与细胞间的信号交流。本课题组发现，胰腺癌细胞大量产生迁移体，并可被巨噬细胞吞噬；蛋白质谱鉴定，胰腺癌迁移体中含有多种影响TAM分化的关键调控因子。本课题拟进一步研究迁移体对胰腺癌微环境中TAM调控的作用及其对胰腺癌恶性行为的影响，探究通过干预迁移体联合吉西他滨作为提高胰腺癌综合治疗效果方案的可能性。

Pancreatic cancer is extremely malignant and lethal. The biomedical research of pancreatic cancer has changed from the study of biological behavior and regulation mechanisms of tumor cells themselves, into the further study of tumor microenvironment and the effects of its change on tumor’s malignant biological behavior. Tumor associated macrophage (TAM) is an important part of the immune microenvironment of pancreatic cancer. Recent reports and our work found that pancreatic cancer could induce TAM into different phenotypes under the certain condition. But the way and the mechanism of the interaction between pancreatic cancer cells and TAM are unclear. Recent studies found that cells from different species could produce a new kind of extracellular organelles, which is named migrasome. It is found that migrasomes could participate into the signal communication between cells. Our group found that pancreatic cancer cells could produce large quantities of migrasomes which could be phagocytized by macrophages. Many key molecules to affect TAM differentiation are found in pancreatic cancer migrasomes by the quantitative mass spectrum method. We will further explore the roles of migrasomes to regulate the phenotypes and functions of pancreatic cancer TAM and its effects on tumor’s malignant biological behavior, and uncover the combination of migrasome intervention and gemcitabine to present new strategies for the integrated treatment of pancreatic cancer.