ArticleNature communications2017
Clonal evolution in myelodysplastic syndromes.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
79 citing papers in PubMed, 141 citations in OpenAlex.
- Long-read sequencing resolvesHaematologica · 2026Article
- Article
- Prognostic value of measurable residual disease in high-risk MDS after intensive chemotherapy in HOVON-SAKK studies.HemaSphere · 2026Article
- B-cell acute lymphoblastic leukemia following myelodysplastic syndromes: a case report and literature review.Journal of hematopathology · 2026Review
- Isolated del(5q) with myeloproliferative driver mutations: A systematic review of published cases and clinical implications.Therapeutic advances in hematology · 2026Review
- Progress in the Genetics of Myelodysplastic Syndromes with a Latin American Perspective.Genes · 2025Review
- [Application of the variant allele frequency of myeloid-associated gene mutations in myelodysplastic syndrome].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025Review
- The Crossroads of Clonal Evolution, Differentiation Hierarchy, and Ontogeny in Leukemia Development.Blood cancer discovery · 2025Review
- Low-risk MDS-A spotlight on precision medicine forHemaSphere · 2025Review
- The Clonal Hematopoiesis-associated GenebioRxiv : the preprint server for biology · 2024Article
- The Bloody Crossroads: Interactions between Periodontitis and Hematologic Diseases.International journal of molecular sciences · 2024Review
- Mutations in myeloid transcription factors and activated signaling genes predict chronic myeloid leukemia outcomes.Blood advances · 2024Article
- Iron overload induces dysplastic erythropoiesis and features of myelodysplasia in Nrf2-deficient mice.Leukemia · 2024Article
- Postazacitidine clone size predicts long-term outcome of patients with myelodysplastic syndromes and related myeloid neoplasms.Blood advances · 2023Article
- The ADAM17 sheddase complex regulator iTAP/Frmd8 modulates inflammation and tumor growth.Life science alliance · 2023Article
- Reconstructing Clonal Evolution-A Systematic Evaluation of Current Bioinformatics Approaches.International journal of environmental research and public health · 2023Article
- The roles of bone remodeling in normal hematopoiesis and age-related hematological malignancies.Bone research · 2023Review
- Emerging treatments for myelodysplastic syndromes: Biological rationales and clinical translation.Cell reports. Medicine · 2023Review
- [Outcome of allogeneic hematopoietic stem cell transplantation in 14 patients with NPM1-mutated myelodysplastic syndromes].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023Article
- clevRvis: visualization techniques for clonal evolution.GigaScience · 2022Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 6 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer development is a dynamic process during which the successive accumulation of mutations results in cells with increasingly malignant characteristics. Here, we show the clonal evolution pattern in myelodysplastic syndrome (MDS) patients receiving supportive care, with or without lenalidomide (follow-up 2.5-11 years). Whole-exome and targeted deep sequencing at multiple time points during the disease course reveals that both linear and branched evolutionary patterns occur with and without disease-modifying treatment. The application of disease-modifying therapy may create an evolutionary bottleneck after which more complex MDS, but also unrelated clones of haematopoietic cells, may emerge. In addition, subclones that acquired an additional mutation associated with treatment resistance (TP53) or disease progression (NRAS, KRAS) may be detected months before clinical changes become apparent. Monitoring the genetic landscape during the disease may help to guide treatment decisions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.