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Temporal genomic dynamics shape clinical trajectory in multiple myeloma
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Abstract
Multiple myeloma evolution is characterized by the accumulation of genomic drivers over time. To unravel this timeline and its impact on clinical outcomes, we analyzed 421 whole-genome sequences from 382 patients. Using clock-like mutational signatures, we estimated a time lag of two to four decades between the initiation of events and diagnosis. We demonstrate that odd-numbered chromosome trisomies in patients with hyperdiploidy can be acquired simultaneously with other chromosomal gains (for example, 1q gain). We show that hyperdiploidy is acquired after immunoglobulin heavy chain translocation when both events co-occur. Finally, patients with early 1q gain had adverse outcomes similar to those with 1q amplification (>1 extra copy), but fared worse than those with late 1q gain. This finding underscores that the 1q gain prognostic impact depends more on the timing of acquisition than on the number of copies gained. Overall, this study contributes to a better understanding of the life history of myeloma and may have prognostic implications.
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Different patients might experience different exposure in time and intensity in the germinal center, potentially reflecting unique interaction with the external environment.
“Importantly, based on the different number of GC mutations observed across hundreds of WGS, it has been shown that different patients might experience different exposure in time and intensity, potentially reflecting unique interaction with the external environment.12,13,15,72,73”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Results sections on study cohorts and mutational signatures report 421 whole-genome sequences and identify SBS9 as a germinal-center-associated signature that was undetectable in 38 patients. This supports variation in the observed germinal-center mutation signal, but the paper does not attribute that variation to differences in time or intensity of germinal-center exposure or to patients’ interactions with the external environment. (LLM, conf=0.82)
Experimental — accuracy not yet measuredInitial development of HY occurs at a very early age, in the 2nd and 3rd decade of life, with acquisition of additional trisomies and aneuploidies in subsequent decades.
“Different independent studies have indicated initial development of HY at a very early age, in 2nd and 3rd decade of life with acquisition of additional trisomies and aneuploidies in subsequent decade.9,10,12,13,15”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Results section, “Age of multiple myeloma initiation in patients’ life” (page unavailable), estimates a median age of 26.5 years for the first large chromosomal gains, consistent with early development in the second or third decade. But “Multiple myeloma molecular time” reports that odd-numbered trisomies occurred in the same time window in 91% of hyperdiploid samples; it does not establish that additional trisomies and aneuploidies are generally acquired in subsequent decades. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe B-cells from which multiple myeloma originates experience prolonged or chronic stimulation in the germinal center.
“In fact, several studies have supported the idea that the B-cells from which MM originate, experience a prolonged/chronic stimulation in the GC.15,40,41,70,71”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Introduction says myeloma likely begins in the germinal center, where a B-cell acquires initiating genomic changes. The Results describe mutational evidence consistent with germinal-center initiation, but neither passage establishes prolonged or chronic stimulation there. The paper’s finding that myeloma can evolve for decades before diagnosis does not establish how long the originating B-cell was stimulated in the germinal center. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe most frequent non-odd HY chromosome is 1q gain.
“The most frequently non-odd HY chromosome is 1q gain. 15”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Results section ‘Multiple myeloma molecular time’ identifies 1q gain as an additional gain in hyperdiploid patients, but does not establish it as the most frequent non-odd gain. Among gains acquired in the same time window as hyperdiploidy, it reports 1q gain in 54 patients and 6p gain in 58. (LLM, conf=0.84)
Experimental — accuracy not yet measuredWhen HY and IGH co-occur (in approximately 10% of patients), HY always occurs after IGH.
“3) when HY and IGH co-occur (in ~10% of patients), HY always occurs after IGH;”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Discussion (page unavailable) says canonical IGH translocations consistently precede hyperdiploidy when they co-occur, supporting the claimed order. It does not give ~10% as the frequency of co-occurrence: the ~10% figure there refers to patients whose trisomies arise stepwise. (LLM, conf=0.87)
Experimental — accuracy not yet measured
MM transformation happens very early in the timeline.
“The fact that alterations like 1q gain can be acquired so early suggests that the MM transformation happens very early in the timeline.15”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Results (Chromosome 1q gain life history; page unavailable) say that 1q gain can arise early or late in myeloma pathogenesis. The Discussion (page unavailable) places myeloma-initiating events decades before diagnosis, but the paper does not establish that transformation to active MM occurs at that early point. The claim conflates early genomic events with early transformation. (LLM, conf=0.85)
Experimental — accuracy not yet measuredSMM that progresses to multiple myeloma has a time of initiation of approximately 30 to 40 years.
“This has been recently supported by several papers, where using molecular mathematical modeling, it has been shown that SMM that progresses to MM has a time of initiation of approximately 30 to 40 years.9,10,12,13,1515”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Results section, “Age of multiple myeloma initiation in patients’ life” (page unavailable), reports a median 32-year lag between the first large chromosomal gains and myeloma diagnosis in 155 newly diagnosed patients. That supports a decades-long timeline, but the estimate is not specifically for SMM patients who progressed to myeloma, and it dates chromosomal gains rather than the onset of SMM. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe existence of three distinct groups is supported by the most recent temporal models and estimates developed using FISH and DNA sequencing on large sample sets.
“The existence of these three distinct groups is supported by the most recent temporal models and estimates developed using FISH and DNA sequencing on large sample sets.9,11,15,79,84”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Introduction and Methods describe a large whole-genome sequencing dataset and FISH analyses, and the Results use molecular timing to distinguish patterns of myeloma evolution. However, the Results discuss 12 genomically defined subgroups, not a temporal model establishing the existence of the three distinct groups claimed here. Page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredAll cases of multiple myeloma are preceded by precursor conditions such as smoldering multiple myeloma and monoclonal gammopathy of undetermined significance, often decades before diagnosis.
“MM is well-described to be universally preceded by precursor states, often decades before it is even diagnosed.”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
Some chromosomes tend to be acquired earlier than others in HY.
“2) some chromosomes tend to be acquired earlier than others;”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
Early 1q is associated with a more aggressive disease.
“Given their prognostic impact on clinical outcomes, we recently explored whether the timing could affect outcomes, and indeed early 1q seems to be associated with a more aggressive disease.15”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
In more than 50% of patients, HY multi-gain events also include other non-odd chromosomes, including 1q gain.
“4) in more than 50% of patients, HY multi-gain events also include other non-odd chromosomes, including 1q gain.”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
Not all HY duplications are acquired at the same time.
“1) not all HY duplications are acquired at the same time;”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
IGH translocations and HY can be identified decades prior to progression.
“The detection of IGH translocations and HY, which can be identified decades prior to progression, reinforcing the concept that MM develops over a protracted time span.15”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
Multiple myeloma develops over a protracted time span.
“reinforcing the concept that MM develops over a protracted time span.15”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
A significant fraction of SMM has already transformed into MM.
“This temporal similarity between progressive SMM and MM further strengthens the hypothesis that a significant fraction of SMM has already transformed into MM.”
From Evolution of Multiple Myeloma from a Genomic Perspective (2026) · cites this paper as [15]
The Introduction describes SMM as an asymptomatic precursor stage, and the Discussion reports that myeloma-initiating events can precede diagnosis by decades. Neither passage says that a significant fraction of SMM has already transformed into MM. Searches for progressive SMM and transformation did not locate that conclusion in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
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Self-citationSuperior detection rate of plasma cell FISH using FACS-FISH
Gagnon, M.-F., Midthun, S. M., Fangel, J. A., Schuh, C. M., Luoma, I. M., Pearce, K. E., Meyer, R. G., Ailawadhi, S., Arribas, M., Braggio, E., et al. (2023) · American Journal of Clinical Pathology · doi:10.1093/ajcp/aqad108 · Cited by 10
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Self-citationPeterson, J. F., Meyer, R. G., Smoley, S. A., Webley, M. R., Smadbeck, J. B., Vasmatzis, G., Pearce, K. E., Greipp, P. T., Ketterling, R. P., Craig, F. E., et al. (2019) · Clinical Lymphoma Myeloma & Leukemia · doi:10.1016/j.clml.2019.06.006 · Cited by 4
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Self-citation
Flagged first, then by citations
Research works printed but not linked: 3
- Bolli, F. et al. Genomic patterns of progression in smoldering multiple myeloma. Nat. Commun. 9, 3363 (2018). · DOI · Paper page
- Walker, B. A. et al. A high-risk, Double-Hit, group of newly diagnosed myeloma identified by genomic analysis. Leukemia 33, 159–170 (2019). · DOI
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Cited by
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Kaddoura, M., Wiedmeier, J. E., Gupta, V. A., Jelinek, T., Ziccheddu, B., Shivaram, S., Tang, H., Owens, R. W., Sevcikova, T., Fonseca, R., et al. (2026) · Blood · doi:10.1182/blood.2025029996 · Cited by 2
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Garcés, J., & Maura, F. (2026) · Blood · doi:10.1182/blood.2025031255
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Ghobrial, I. M., Perron, N., Aranha, M. P., Wu, T., Pantano, L., Yue, H., Lightbody, E. D., Saha, R., Rahmat, M., Timonian, M., et al. (2026) · Research Square · doi:10.21203/rs.3.rs-9226435/v1
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Koops, M., Bertamini, L., Papazian, N., Korst, C. L. B. M., Budai, M. J., Hoogenboezem, R. M., Sanders, M. A., van der Holt, B., van Duin, M., Broijl, A., et al. (2026) · Blood Cancer Discovery · doi:10.1158/2643-3230.bcd-26-0080
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Zeng, Z., Lu, J., Shang, J., 游, 鸿., Wang, Q., Wen, L., Wang, Q., Yan, W., Wu, C., Wang, P., et al. (2026) · British Journal of Haematology · doi:10.1111/bjh.70817
Metadata
- Authors
- Maura, F., Kaddoura, M., Poos, A. M., Baughn, L. B., Ziccheddu, B., Bärtsch, M.-A., Cirrincione, A., Maclachlan, K., Chojnacka, M., Diamond, B., Papadimitriou, M., Blaney, P., John, L., Reichert, P., Huhn, S., Gagler, D., Zhang, Y., Dogan, A., Lesokhin, A. M., Davies, F., Goldschmidt, H., Fenk, R., Weisel, K. C., Mai, E. K., Korde, N., Morgan, G. J., Rajkumar, S. V., Kumar, S., Usmani, S., Landgren, O., Raab, M. S., & Weinhold, N.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- University of Miami (US)
- German Cancer Research Center (DE)
- Mayo Clinic (US)
- NYU Langone Health (US)
- Heidelberg University (DE)
- University Hospital Heidelberg (DE)
- Düsseldorf University Hospital (DE)
- University Medical Center Hamburg-Eppendorf (DE)
- Corresponding author
- Maura, Francesco
- Weinhold, Niels
- ORCID
- Maura, Francesco
- Kaddoura, Marcella
- Poos, Alexandra M.
- Baughn, Linda B.
- Ziccheddu, Bachisio
- Cirrincione, Anthony
- Maclachlan, Kylee
- Chojnacka, Monika
- Diamond, Benjamin
- Papadimitriou, Marios
- Blaney, Patrick
- John, Lukas
- Reichert, Philipp
- Huhn, Stefanie
- Gagler, Dylan
- Zhang, Yanming
- Dogan, Ahmet
- Lesokhin, Alexander M.
- Davies, Faith
- Goldschmidt, Hartmut
- Fenk, Roland
- Weisel, Katja C.
- Mai, Elias K.
- Korde, Neha
- Morgan, Gareth J.
- Rajkumar, S. Vincent
- Kumar, Shaji
- Usmani, Saad
- Landgren, Ola
- Raab, Marc S.
- Weinhold, Niels
- Venue
- Nature Genetics
- Published
- 2025-08-20
- Volume
- 57
- Issue
- 9
- Pages
- 2203-2214
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC13127375
- OpenAlex
- W4413337884
- Cited by
- 14
- References
- 91
- Citations by year
- 2026: 9 · 2025: 4
- FWCI
- 9.61
- Type
- journal article
- Language
- en
- Open access
- Licence
- Locations
- Nature Genetics (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Cancer Institute (P30 CA 240139, P30 CA 008748)
- 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 › Hematology › Acute Myeloid Leukemia Research
- Keywords
- multiple myeloma, tumor evolution, mutational signatures, hyperdiploidy, 1q gain, 1q amplification, chromosomal gains, prognosis, whole genome sequencing
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