Mechanisms of GPRC5D loss mediating resistance to anti-GPRC5D CAR T therapy. In the T-cell therapy–naive setting, GPRC5D is highly expressed on multiple myeloma (MM) tumor cells, enabling effective targeting by anti-GPRC5D CAR T cells (arrows hitting the bullseye). After relapse, tumor cells evade immune recognition through loss of GPRC5D, making anti-GPRC5D CAR T therapy ineffective. Mechanisms of GPRC5D antigen escape include genomic deletion of the GPRC5D locus and epigenetic silencing via promoter/enhancer methylation. CAR, chimeric antigen receptor. Figure generated using BioRender.

Mechanisms of GPRC5D loss mediating resistance to anti-GPRC5D CAR T therapy. In the T-cell therapy–naive setting, GPRC5D is highly expressed on multiple myeloma (MM) tumor cells, enabling effective targeting by anti-GPRC5D CAR T cells (arrows hitting the bullseye). After relapse, tumor cells evade immune recognition through loss of GPRC5D, making anti-GPRC5D CAR T therapy ineffective. Mechanisms of GPRC5D antigen escape include genomic deletion of the GPRC5D locus and epigenetic silencing via promoter/enhancer methylation. CAR, chimeric antigen receptor. Figure generated using BioRender.

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