Grant: Project Grant

Cachexia, the rapid loss of muscle mass, is a hallmark of cancer and a major contributor to cancer related death. Currently there are no therapies to mitigate this problem. It is thought that cancers cause cachexia by producing factors that act directly on muscle cells. However, we have evidence that suggests a non-muscle cell type resident in muscle tissue, called fibroadipogenic progenitors, may act as an intermediate, receiving signals from the cancer and causing loss of muscle. Fibroadipogenic progenitors (FAP) are required for muscle regeneration, a process that is inhibited in cachexia. They are also required for the maintenance of muscle mass in the long term. Finally they are important in determining the inflammatory environment of muscle. Here, we propose to investigate how they respond to pancreatic cancer, which is a common cause of cachexia. We will investigate how the cancer changes FAP functions, and how this impact muscle. Through this effort we will provide a better understanding of how cachexia is induced, and reveal new targets for therapeutic intervention aimed at preserving muscle mass and increasing the survival of cancer patients.