Director, RNAi & CRISPR Core lab Memorial Sloan-Kettering Cancer Center
Disclosure: Disclosure information not submitted.
Metastatic cancers relapse due to the emergence of stem-like clones capable of reversible quiescence, tumor re-initiation, and therapy resistance-termed metastasis initiating cells (MICs).
This tutorial will cover our work with organoid cultures, which underscores the distinct requirements of the CSCs that initiate tumor growth, and MICs that drive lethal metastatic relapse. We identify the loss of epithelial integrity, an obligatory step of metastasis, as a crucial molecular driver of the transcriptional plasticity required for the emergence of pro-metastatic traits. Further, we define L1CAM as a crucial vulnerability of MICs that could be exploited therapeutically to treat patients with metastatic cancer.