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CD38-negative relapse in multiple myeloma after daratumumab-based chemotherapy
J. Minarik, M. Novak, P. Flodr, J. Balcarkova, M. Mlynarcikova, P. Krhovska, T. Pika, Z. Pikalova, J. Bacovsky, V. Scudla,
Language English Country Great Britain
Document type Case Reports
PubMed
28470777
DOI
10.1111/ejh.12902
Knihovny.cz E-resources
- MeSH
- ADP-ribosyl Cyclase 1 antagonists & inhibitors metabolism MeSH
- Biomarkers MeSH
- Molecular Targeted Therapy MeSH
- Cytogenetic Analysis MeSH
- Immunophenotyping MeSH
- Middle Aged MeSH
- Humans MeSH
- Multiple Myeloma diagnosis drug therapy genetics metabolism MeSH
- Antibodies, Monoclonal MeSH
- Prognosis MeSH
- Antineoplastic Combined Chemotherapy Protocols therapeutic use MeSH
- Recurrence MeSH
- Comparative Genomic Hybridization MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Case Reports MeSH
We present a case report of a patient relapsing after anti-CD38 treatment (daratumumab). The phenotype of the disease changed during this treatment, and the myeloma clone became CD38 negative and daratumumab refractory. We expected clonal shift, however, based on immunophenotyping, cytogenetics and arrayCGH; the clone was identical as before daratumumab-based treatment with the exception of CD38 negativity. We suggest that the downregulation or loss of CD38 might be an epigenetic "escape mechanism" of malignant plasma cells from antibody-based treatment. The aim of our study was to point out the pitfalls of immunophenotyping and cytogenetics in both assessing the minimal residual disease and clone detection after monoclonal antibody-based therapy.
References provided by Crossref.org
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- $a We present a case report of a patient relapsing after anti-CD38 treatment (daratumumab). The phenotype of the disease changed during this treatment, and the myeloma clone became CD38 negative and daratumumab refractory. We expected clonal shift, however, based on immunophenotyping, cytogenetics and arrayCGH; the clone was identical as before daratumumab-based treatment with the exception of CD38 negativity. We suggest that the downregulation or loss of CD38 might be an epigenetic "escape mechanism" of malignant plasma cells from antibody-based treatment. The aim of our study was to point out the pitfalls of immunophenotyping and cytogenetics in both assessing the minimal residual disease and clone detection after monoclonal antibody-based therapy.
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