Host immature myeloid cells in tumor suppressor or promoter roles of TGFbeta

在过去的一年里，我们取得了稳步进展。我们已经建立和培育了宿主未成熟髓系细胞中TGFbeta R2受体特异性缺失的小鼠克隆。我们观察到髓系TGFbeta R2 Ko小鼠的肿瘤进展显著减缓。我们获得了涉及全身免疫反应的机械性见解，以及髓系细胞与微环境和远处转移器官中的肿瘤细胞的直接相互作用。我们已经确定miRNA130a和miRNA145直接靶向髓系TGFbeta R2及其相关的信号网络IGFR途径。我们希望利用所获得的研究信息开发新的翻译机会。我们正在利用技术核心资源，并为这个项目与几个实验室合作。

We have made steady progress in the past year. We have produced and bred mouse colonies in which TGFbeta R2 receptor is specifically deleted in host immature myeloid cells. We have observed significantly decreased tumor progression in myeloid TGFbeta R2 ko mice. We obtained mechanistic insight that involves systemic immune response as well as direct interaction of myeloid cells with tumor cells in the microenvironment and distant metastatic organ. We have identified that miRNA130a and miRNA145 directly target myeloid TGFbeta R2 and its associated signaling networks the IGFR pathway. We hope to develop new translational opportunities with the research information obtained. We are utilizing technical core resources and collaborating with several labs for this project.