ArticleNature communications2019
Invariant patterns of clonal succession determine specific clinical features of myelodysplastic syndromes.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 69 citations in OpenAlex.
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- DifferentCancers · 2026Article
- Predicting secondary myeloid neoplasms in acquired aplastic anemia using machine learning models.Blood neoplasia · 2025Article
- IMOP-Cancer: identifying mutation order pairs impacting cancer phenotypes.Briefings in bioinformatics · 2025Article
- Comprehensive Age-Stratified Impact ofCancers · 2025Article
- Clonal hematopoiesis in large granular lymphocytic leukemia.Leukemia · 2025Article
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- Mutation order in acute myeloid leukemia identifies uncommon patterns of evolution and illuminates phenotypic heterogeneity.Leukemia · 2024Article
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- Discovery of U2AF1 neoantigens in myeloid neoplasms.Journal for immunotherapy of cancer · 2023Article
- The clinicopathologic significance of NPM1 mutation and ability to detect mutated NPM1 by immunohistochemistry in non-AML myeloid neoplasms.Genes, chromosomes & cancer · 2023Article
- Clonal evolution and hierarchy in myeloid malignancies.Trends in cancer · 2023Review
- Novel scheme for defining the clinical implications of TP53 mutations in myeloid neoplasia.Journal of hematology & oncology · 2023Article
- Leukemia relapse via genetic immune escape after allogeneic hematopoietic cell transplantation.Nature communications · 2023Article
- Molecular patterns identify distinct subclasses of myeloid neoplasia.Nature communications · 2023Article
- Microenvironmental control of hematopoietic stem cell fate via CXCL8 and protein kinase C.Cell reports · 2023Article
- Article
Corrections and comments
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Authors and funding
24 authors at 5 institutions in 3 countries.
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Abstract
Myelodysplastic syndromes (MDS) arise in older adults through stepwise acquisitions of multiple somatic mutations. Here, analyzing 1809 MDS patients, we infer clonal architecture by using a stringent, the single-cell sequencing validated PyClone bioanalytic pipeline, and assess the position of the mutations within the clonal architecture. All 3,971 mutations are grouped based on their rank in the deduced clonal hierarchy (dominant and secondary). We evaluated how they affect the resultant morphology, progression, survival and response to therapies. Mutations of SF3B1, U2AF1, and TP53 are more likely to be dominant, those of ASXL1, CBL, and KRAS are secondary. Among distinct combinations of dominant/secondary mutations we identified 37 significant relationships, of which 12 affect clinical phenotypes, 5 cooperatively associate with poor prognosis. They also predict response to hypomethylating therapies. The clonal hierarchy has distinct ranking and the resultant invariant combinations of dominant/secondary mutations yield novel insights into the specific clinical phenotype of MDS.
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