ArticleBlood advances2021
Single- and double-hit events in genes encoding immune targets before and after T cell-engaging antibody therapy in MM.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 81 citations in OpenAlex.
- Distinct epitope engagement confers differential activity of linvoseltamab vs teclistamab across BCMA mutations.Blood advances · 2026Article
- Navigating the Therapeutic Landscape of Multiple Myeloma: Immunotherapy, Microenvironment, and Resistance.Biomedicines · 2026Review
- Promoter hypermethylation as a reversible mechanism of resistance to GPRC5D-directed therapy in multiple myeloma.Haematologica · 2026Article
- Sustained disease remission after a limited duration of bispecific antibody therapy in patients with multiple myeloma.HemaSphere · 2026Article
- Loss of GPRC5D enhances the proliferative capacity and competitive fitness of myeloma upon anti-GPRC5D immunotherapy.Leukemia · 2026Article
- Outcomes of Double-Hit and Single High-Risk Cytogenetic Newly Diagnosed Myeloma in Transplant-Eligible Patients.Current oncology (Toronto, Ont.) · 2026Article
- Dynamics of BCMA expression in patients with relapsed/refractory multiple myeloma receiving BCMA-directed CAR-T therapy.Blood cancer journal · 2026Article
- The evolution to hepta-refractory myeloma involves sequential loss of CD38, BCMA and GPRC5D.Leukemia · 2026Article
- Multimodal antigenic escape to GPRC5D-targeted T cell engagers in multiple myeloma.Nature medicine · 2026Article
- Poor outcomes with BCMA-targeting bispecific antibodies following early relapse from ide-cel: a real-world French study.Blood advances · 2026Article
- Pathways of Resistance: Modern Multiple Myeloma Therapies and Overcoming Reliance on Genomic Integrity.International journal of molecular sciences · 2026Review
- Article
- Emerging precision medicine in multiple myeloma: clinical and preclinical landscape of T cell, natural killer cell, and macrophages engaging multi-specific antibodies.Frontiers in immunology · 2026Review
- Solving Riddles Through Sequencing (SIRIUS): unlocking hematologic diagnoses by whole genome and transcriptome sequencing.Leukemia · 2026Article
- Antibody-Drug Conjugates, T-Cell Engager Bispecific Antibodies and Chimeric Antigen Receptor T Cells for Multiple Myeloma: What's the Current Status?Targeted oncology · 2026Review
- Teclistamab for Relapsed or Refractory Multiple Myeloma: A Review of Efficacy, Safety, Resistance Mechanisms and Future Directions.Biologics : targets & therapy · 2026Review
- Article
- Unique molecular assay (UMA): a next-generation sequencing targeted panel for efficient and comprehensive genomic profiling and risk stratification of multiple myeloma.Haematologica · 2025Article
- Biallelic antigen escape is a mechanism of resistance to anti-CD38 antibodies in multiple myeloma.Blood · 2025Article
- Genetic and epigenetic mechanisms of GPRC5D loss after anti-GPRC5D CAR T-cell therapy in multiple myeloma.Blood · 2025Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell-engaging immunotherapies exert unprecedented single-agent activity in multiple myeloma (MM), thereby putting a yet unexplored selective pressure on the clonal architecture. In this study, we report on homozygous BCMA (TNFRSF17) gene deletion after BCMA-targeting T cell-redirecting bispecific antibody therapy in a heavily pretreated MM patient. Loss of BCMA protein expression persisted over subsequent relapses, with no response to treatment with anti-BCMA antibody drug conjugate. In light of the multiple alternative targets that are emerging in addition to BCMA, we extended our analyses to delineate a more complete picture of genetic alterations that may have an impact on immunotherapy targets in MM. We performed whole-genome sequencing and RNA sequencing in 100 MM patients (50 were newly diagnosed; 50 were relapsed/refractory) and identified a significant proportion of patients with aberrations in genes encoding immunotherapy targets; GPRC5D ranked first with 15% heterozygous deletions, followed by CD38 (10%), SDC1 (5%), and TNFRSF17 (4%). Notably, these heterozygous deletions did not lower the expression levels of respective genes, but they may represent a first hit that drives the acquisition of homozygous deletions and subsequent antigen-loss relapse upon targeted immunotherapy. In summary, we show preexisting vulnerability in genes encoding immunotargets before and homozygous deletions after T cell-engaging immunotherapy.
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