ArticleNature genetics2017
Dynamics of clonal evolution in myelodysplastic syndromes.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 275 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
275 citing papers in PubMed, 1 synthesis or guideline pooled it, 417 citations in OpenAlex.
- Comparison and Implications of Mutational Profiles of Myelodysplastic Syndromes, Myeloproliferative Neoplasms, and Myelodysplastic/Myeloproliferative Neoplasms: A Meta-Analysis.Frontiers in oncology · 2020Pooled it
- Clinical significance of chromatin-spliceosome acute myeloid leukemia: a report from the Northern Italy Leukemia Group (NILG) randomized trial 02/06.Haematologica · 2021Trial
- Sensitivity to ATR-CHK1 pathway inhibition in MDS/AML is enhanced by SRSF2 mutations and reduced by RUNX1 loss.Leukemia · 2026Article
- Long-term mutational analysis, clonal metrics, and dynamics in patients with chronic idiopathic neutropenia.HemaSphere · 2026Article
- ELN vs. IPSS-M in MDS/AML: Which Prognostic System Should Guide Clinical Decision-Making?Cancers · 2026Review
- IDH1- and IDH2-mutated myeloid neoplasms: mutational pattern, clonal hierarchy, and the role in AML transformation.Blood advances · 2026Article
- Exposure to Agent Orange and association with myelodysplastic syndromes.Blood advances · 2026Article
- Trisomy 8 alters chromatin conformations and activates Y chromosome genes in stem cells to drive a pre-leukemic state.Oncogene · 2026Article
- Review
- U2AF regulates the translation and localization of nuclear-encoded mitochondrial mRNAs.Molecular cell · 2026Article
- Case report: Dynamic genetic profiles reveal a patient with myelodysplastic neoplasm transforming into acute myeloid leukemia.Discover oncology · 2026Article
- Modeling the evolutionary dynamics of clonal hematopoiesis.Nature genetics · 2026Review
- B-cell acute lymphoblastic leukemia following myelodysplastic syndromes: a case report and literature review.Journal of hematopathology · 2026Review
- The global epidemiology of acute myeloid leukaemia.Nature reviews. Clinical oncology · 2026Review
- Therapeutic targeting of chromatin alterations in leukemia and solid tumors.International journal of cancer · 2026Review
- [Chinese expert consensus on the clinical application of next-generation sequencing technology in myelodysplastic neoplasms (2026)].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- Article
- Article
- Chromatin accessibility in stem cells unveils progressive transcriptional alterations in myelodysplastic syndrome.Nature communications · 2025Article
- Advances in measurable residual disease assessment for acute myeloid leukemia: from cytogenetics and molecular biology to assessment of the methylation pattern and surface-enhanced Raman scattering as emerging technologies.Biomarker research · 2025Review
215 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
37 authors at 10 institutions in 4 countries.
Funding
Abstract
To elucidate differential roles of mutations in myelodysplastic syndromes (MDS), we investigated clonal dynamics using whole-exome and/or targeted sequencing of 699 patients, of whom 122 were analyzed longitudinally. Including the results from previous reports, we assessed a total of 2,250 patients for mutational enrichment patterns. During progression, the number of mutations, their diversity and clone sizes increased, with alterations frequently present in dominant clones with or without their sweeping previous clones. Enriched in secondary acute myeloid leukemia (sAML; in comparison to high-risk MDS), FLT3, PTPN11, WT1, IDH1, NPM1, IDH2 and NRAS mutations (type 1) tended to be newly acquired, and were associated with faster sAML progression and a shorter overall survival time. Significantly enriched in high-risk MDS (in comparison to low-risk MDS), TP53, GATA2, KRAS, RUNX1, STAG2, ASXL1, ZRSR2 and TET2 mutations (type 2) had a weaker impact on sAML progression and overall survival than type-1 mutations. The distinct roles of type-1 and type-2 mutations suggest their potential utility in disease monitoring.
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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.