Retention of CD19 intron 2 contributes to CART-19 resistance in leukemias with subclonal frameshift mutations in CD19
Summary This study identifies intron 2 retention in CD19 transcripts as a mechanism contributing to CAR-T19 therapy resistance in leukemias harboring subclonal frameshift mutations in CD19. The findings reveal how alternative splicing can undermine antigen-targeted cancer immunotherapy.