Targeting epithelial plasticity in pancreatic cancer (P12)

针对胰腺癌的上皮可塑性（P12）

• 批准号: 403831884
• 金额: --
• 依托单位: Lehrstuhl für Zellbiophysik
• 依托单位国家: 德国
• 项目类别: Collaborative Research Centres
• 财政年份: 2018
• 资助国家: 德国
• 起止时间: 2017-12-31 至 2022-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/403831884?language=en
• 关键词: Targeting; epithelial; plasticity; pancreatic; cancer

Cellular plasticity drives tumour initiation, metastatic dissemination as well as resistance to therapy. The molecular programs orchestrating plasticity are poorly defined. We have generated a novel PDAC organoid morphogenesis system which allows us to capture tumour plasticity and heterogeneity in a dynamic fashion in vitro. This organoid assay will be employed to determine the underlying molecular mechanisms and to delineate the impact of cellular mechanics as well as to define strategies to inhibit tumour plasticity with the ultimate goal to overcome adaptive resistance towards chemotherapy in pancreatic cancer.

细胞可塑性驱动肿瘤的起始、转移性传播以及对治疗的抵抗。调控可塑性的分子程序定义不清。我们已经产生了一种新的PDAC类器官形态发生系统，使我们能够在体外以动态的方式捕捉肿瘤的可塑性和异质性。这种类器官试验将用于确定潜在的分子机制，描述细胞力学的影响，并确定抑制肿瘤可塑性的策略，最终目标是克服胰腺癌对化疗的适应性耐药。