Cell state plasticity is required for metastatic tumor growth in FN-RMS
Rhabdomyosarcoma (RMS) is a common cancer found in children and young adults. This cancer shares many characteristics with muscle, and the most common type is called fusion-negative RMS (FN-RMS), which is the subject of my work. While patients with RMS often have good outcomes, those whose cancer has spread (metastasized) face a very poor prognosis, with less than 20% surviving. This highlights the urgent need to understand how RMS spreads and eventually kills patients. Our recent research using advanced techniques to study individual cancer cells has revealed that RMS tumors contain at least three different types of cells, similar to those found in normal muscle development. Surprisingly, we identified that not all cell types have the capability to cause metastatic cancer, and the cell type which most resembles mature muscle cells is most metastatic. In this project, I will uncover how FN-RMS spreads to other parts of the body.
Project Goals
I will first identify which types of cancer cells are responsible for starting new tumors in distant organs. Next, I will test how different cell types, and their ability to change from one type to another, contribute to each step of the spread. Finally, I will uncover the key molecular signals that allow cancer cells to regrow once they have reached a new site. The ultimate goal of my work is to discover new ways to prevent RMS from spreading and to improve treatment for patients whose cancer has already spread. This could lead to the development of new therapies and better ways to predict which patients are at higher risk of their cancer spreading.
