Journal
NATURE MEDICINE
Volume 27, Issue 4, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41591-021-01245-5
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Funding
- German Cancer Aid via the MSNZ program
- IZKF Wurzburg
- DFG [SFB/TR 221 project A3]
- German Research Society graduate college [2157]
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BCMA serves as a target for immunotherapies and a biomarker for tumor load in MM. The study found a correlation between TNFRSF17 loss and BCMA loss, leading to immune escape. Heterozygous TNFRSF17 deletion at baseline in high hyperhaploid MM patients may increase the risk of BCMA loss after immunotherapy.
B cell maturation antigen (BCMA) is a target for various immunotherapies and a biomarker for tumor load in multiple myeloma (MM). We report a case of irreversible BCMA loss in a patient with MM who was enrolled in the KarMMa trial (NCT03361748) and progressed after anti-BCMA CAR T cell therapy. We identified selection of a clone with homozygous deletion of TNFRSF17 (BCMA) as the underlying mechanism of immune escape. Furthermore, we found heterozygous TNFRSF17 loss or monosomy 16 in 37 out of 168 patients with MM, including 28 out of 33 patients with hyperhaploid MM who had not been previously treated with BCMA-targeting therapies, suggesting that heterozygous TNFRSF17 deletion at baseline could theoretically be a risk factor for BCMA loss after immunotherapy.
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