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When a cancer treated with a therapy aimed at one surface marker (CD19, BCMA, HER2) survives by shedding that marker, so the drug has nothing to grab. About a third of relapses after CD19 CAR-T are antigen-negative.
Mechanisms include mutations or splice variants that remove the epitope, deletion of the gene (TNFRSF17/BCMA biallelic loss in myeloma), lineage switch (B-ALL relapsing as myeloid leukaemia under CD19 pressure), trogocytosis (CAR-T cells stripping antigen off tumour cells), and pre-existing antigen-low subclones. Responses are dual-targeting CARs (CD19/CD22, BCMA/GPRC5D), sequencing to a different antigen (GPRC5D or FcRH5 after BCMA), logic-gated CARs and antigen-independent strategies. It is distinct from T-cell-intrinsic failure (exhaustion, poor persistence), which is the other main cause of relapse, and flow cytometry at relapse distinguishes the two.
In plain words · CD19 is a marker on B cells and B-cell cancers, and was the target of the first CAR-T therapies ever approved.
Showing the target this term concerns: CD19.
The glossary entry explains the word; the readout page carries the scoring rule, the thresholds approvals use, the companion diagnostics and the tests.
Shares GPRC5D expression, BCMA expression, Flow cytometry (immunophenotyping).
Shares CD20 expression (CD20-positive), CD19 expression (CD19-positive), Drug resistance (primary and acquired), CD19.
Shares GPRC5D expression, BCMA expression.
Shares BCMA, Drug resistance (primary and acquired), CD19, T-cell engagers (bispecific).
Shares BCMA, CD19, CAR-T cell therapy.
Shares BCMA, CD19, CAR-T cell therapy.
Shares BCMA, CD19, T-cell engagers (bispecific).
Shares CD20 expression (CD20-positive), CD19 expression (CD19-positive), CD19, T-cell engagers (bispecific).