KDM6A Epigenetically Regulates Subtype Plasticity in Small Cell Lung Cancer

Using a CRISPR-based autochthonous SCLC genetically engineered mouse model to study the consequences of KDM6A/UTX inactivation, investigators showed that KDM6A inactivation induced plasticity from ASCL1 to NEUROD1 resulting in SCLC tumors that express both ASCL1 and NEUROD1.