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Single-cell multi-omics of relapse/refractory multiple myeloma patients (Hipo K08K/H067/K43R)

Therapy resistance in cancers is ingrained in complex clonal dynamics. While the major clonal population in a tumour might respond well to the employed intervention, minor clones will eventually mutate, consequently acquiring a selective advantage and drug resistance. Hence, to improve cancer therapy, it is crucial to understand the mechanisms behind clonal evolution. Here, we applied single-cell transcriptomics and epigenomics, as well as whole-genome sequencing to 15 patients with relapsed/refractory multiple myeloma (RRMM). By profiling longitudinal samples throughout varying treatment regimens, we were able to interrogate patterns of evolution across patients. In particular, by defining clones based on copy number aberrations (CNAs), we found evidence for the majority of clones being diminished but not fully eradicated during treatment.

Click on a Dataset ID in the table below to learn more, and to find out who to contact about access to these data

Dataset ID Description Technology Samples
EGAD00001009679 HiSeq X Ten Illumina HiSeq 4000 1
EGAD00001009680 HiSeq X Ten Illumina HiSeq 2000 Illumina HiSeq 4000 30
EGAD00001009681 Illumina HiSeq 4000 2
EGAD00001009682 HiSeq X Ten Illumina NovaSeq 6000 45
EGAD00001009683 Illumina NovaSeq 6000 29
Publications Citations
Resolving therapy resistance mechanisms in multiple myeloma by multiomics subclone analysis.
Blood 142: 2023 1633-1646
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