APOBEC family mutational signatures are associated with poor prognosis translocations in multiple myeloma
Open accessAbstract
We have sequenced 463 presenting cases of myeloma entered into the UK Myeloma XI study using whole exome sequencing. Here we identify mutations induced as a consequence of misdirected AID in the partner oncogenes of IGH translocations, which are activating and associated with impaired clinical outcome. An APOBEC mutational signature is seen in 3.8% of cases and is linked to the translocation-mediated deregulation of MAF and MAFB, a known poor prognostic factor. Patients with this signature have an increased mutational load and a poor prognosis. Loss of MAF or MAFB expression results in decreased APOBEC3B and APOBEC4 expression, indicating a transcriptional control mechanism. Kataegis, a further mutational pattern associated with APOBEC deregulation, is seen at the sites of the MYC translocation. The APOBEC mutational signature seen in myeloma is, therefore, associated with poor prognosis primary and secondary translocations and the molecular mechanisms involved in generating them. Rearrangements of the Ig loci are essential for generating antibody diversity but abnormal translocations can be a driving event for myeloma. Here Walker et al. perform whole exome sequencing on myeloma patients to capture the diversity of mutational changes.
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In MGUS and SMM, MAFB translocations associate with high-risk genomic features but do not always predict progression.
“In the context of MGUS and SMM, these translocations still associate with high-risk genomic features,59,97,98 but strangely do not always predict progression as one might expect.9,90,99”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [97]
The Discussion (page unavailable) says t(14;20), the MAFB translocation, is associated with a long time to progression in MGUS and asymptomatic myeloma, supporting the progression point. It links the adverse translocation subgroups to high mutation load in myeloma, but does not establish that MGUS or SMM cases carrying them have high-risk genomic features. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMAFB translocations are associated with poor outcomes, genomic complexity, and hyper-APOBEC in MM.
“MAFB translocations are known to be associated with poor outcomes, genomic complexity, and hyper-APOBEC in MM.”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [97]
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APOBEC: From mutator to editor
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Self-citationMoving From Cancer Burden to Cancer Genomics for Smoldering Myeloma
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Genomic Instability in Multiple Myeloma
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Self-citationTargeting Translation of mRNA as a Therapeutic Strategy in Cancer
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Evolution and structure of clinically relevant gene fusions in multiple myeloma
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Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer
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Self-citationRole of 1q21 in Multiple Myeloma: From Pathogenesis to Possible Therapeutic Targets
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Dysregulated APOBEC3G causes DNA damage and promotes genomic instability in multiple myeloma
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Self-citationPerspectives on the Risk-Stratified Treatment of Multiple Myeloma
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Chromothripsis as a pathogenic driver of multiple myeloma
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Self-citationAPOBEC3B is an enzymatic source of molecular alterations in esophageal squamous cell carcinoma
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Genome Instability in Multiple Myeloma: Facts and Factors
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The Prognostic Role of MYC Structural Variants Identified by NGS and FISH in Multiple Myeloma
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- Authors
- Walker, B. A., Wardell, C. P., Murison, A., Boyle, E. M., Begum, D. B., Dahir, N. M., Proszek, P. Z., Melchor, L., Pawlyn, C., Kaiser, M. F., Johnson, D. C., Qiang, Y.-W., Jones, J. R., Cairns, D. A., Gregory, W. M., Owen, R. G., Cook, G., Drayson, M. T., Jackson, G. H., Davies, F. E., & Morgan, G. J.
- Affiliations
- Institute of Cancer Research (GB)
- University of Arkansas for Medical Sciences (US)
- University of Leeds (GB)
- University of Birmingham (GB)
- Newcastle University (GB)
- Corresponding author
- Walker, Brian A.
- Morgan, Gareth J.
- ORCID
- Venue
- Nature Communications
- Published
- 2015-04-23
- Volume
- 6
- Issue
- 1
- Pages
- 6997-6997
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4568299
- OpenAlex
- W2059995794
- Cited by
- 313
- References
- 49
- Citations by year
- 2026: 14 · 2025: 23 · 2024: 20 · 2023: 22 · 2022: 48 · 2021: 46 · 2020: 32 · 2019: 29 · 2018: 22 · 2017: 31 · 2016: 19 · 2015: 6
- FWCI
- 20.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Heart of England NHS Foundation Trust
- Cancer Research UK (A17761, A9941, A12136, A10410, A14261)
- University of Leeds
- University of Nottingham
- Medical Research Council (MR/L01629X/1)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- multiple myeloma, APOBEC mutational signature, APOBEC3B, AID, IGH translocation, MYC translocation, MAF, MAFB, kataegis, mutational load, prognosis, transcriptional regulation
- MeSH terms
- Adult, Aged, Aged, 80 and over, Cytidine Deaminase, Female, Humans, Male, Middle Aged, Multiple Myeloma, Mutation, Prognosis, Translocation, Genetic, Minor Histocompatibility Antigens, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-myc, Gene Expression Profiling, Proto-Oncogene Proteins c-maf, MafB Transcription Factor
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