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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,
Jazyk angličtina Země Velká Británie
Typ dokumentu kazuistiky
PubMed
28470777
DOI
10.1111/ejh.12902
Knihovny.cz E-zdroje
- MeSH
- antigeny CD38 antagonisté a inhibitory metabolismus MeSH
- biologické markery MeSH
- cílená molekulární terapie MeSH
- cytogenetické vyšetření MeSH
- imunofenotypizace MeSH
- lidé středního věku MeSH
- lidé MeSH
- mnohočetný myelom diagnóza farmakoterapie genetika metabolismus MeSH
- monoklonální protilátky MeSH
- prognóza MeSH
- protokoly protinádorové kombinované chemoterapie terapeutické užití MeSH
- recidiva MeSH
- srovnávací genomová hybridizace MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- Publikační typ
- kazuistiky 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.
Citace poskytuje 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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