ArticleBlood cancer discovery2022
Convergent Clonal Evolution of Signaling Gene Mutations Is a Hallmark of Myelodysplastic Syndrome Progression.
Article in Blood cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Acute Myeloid Leukemia with Myelodysplasia-Related Gene Mutations.Journal of clinical medicine · 2026Review
- Prognostic value of measurable residual disease in high-risk MDS after intensive chemotherapy in HOVON-SAKK studies.HemaSphere · 2026Article
- Modeling the evolutionary dynamics of clonal hematopoiesis.Nature genetics · 2026Review
- [Myelodysplastic neoplasms with acute myeloid leukemia-like mutations: clinical features, molecular profiles, and prognosis].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025Article
- A heterozygous CEBPA mutation disrupting the bZIP domain in a RUNX1 and SRSF2 mutational background causes MDS disease progression.Nature communications · 2025Article
- Progress in the Genetics of Myelodysplastic Syndromes with a Latin American Perspective.Genes · 2025Review
- Monitoring clonal burden as an alternative to blast count for myelodysplastic neoplasm treatment response.Leukemia · 2025Article
- Article
- Article
- A Brief Overview of the Molecular Landscape of Myelodysplastic Neoplasms.Current oncology (Toronto, Ont.) · 2024Review
- Single-cell Multiomics Analysis of Myelodysplastic Syndromes and Clinical Response to Hypomethylating Therapy.Cancer research communications · 2024Article
- Discovery of U2AF1 neoantigens in myeloid neoplasms.Journal for immunotherapy of cancer · 2023Article
- Emerging Insights into Molecular Mechanisms of Inflammation in Myelodysplastic Syndromes.Biomedicines · 2023Review
- Moving toward a conceptualization of measurable residual disease in myelodysplastic syndromes.Blood advances · 2023Article
- Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia.Blood cancer discovery · 2023Article
- Novel Molecular Insights into Leukemic Evolution of Myeloproliferative Neoplasms: A Single Cell Perspective.International journal of molecular sciences · 2022Review
- Distinct Patterns of Clonal Evolution Drive Myelodysplastic Syndrome Progression to Secondary Acute Myeloid Leukemia.Blood cancer discovery · 2022Article
- Rise of the Clones: Myelodysplastic Syndrome to Secondary Acute Myeloid Leukemia.Blood cancer discovery · 2022Article
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24 authors at 2 institutions in 1 country.
Funding
Abstract
Progression from myelodysplastic syndromes (MDS) to secondary acute myeloid leukemia (AML) is associated with the acquisition and expansion of subclones. Our understanding of subclone evolution during progression, including the frequency and preferred order of gene mutation acquisition, remains incomplete. Sequencing of 43 paired MDS and secondary AML samples identified at least one signaling gene mutation in 44% of MDS and 60% of secondary AML samples, often below the level of standard sequencing detection. In addition, 19% of MDS and 47% of secondary AML patients harbored more than one signaling gene mutation, almost always in separate, coexisting subclones. Signaling gene mutations demonstrated diverse patterns of clonal evolution during disease progression, including acquisition, expansion, persistence, and loss of mutations, with multiple patterns often coexisting in the same patient. Multivariate analysis revealed that MDS patients who had a signaling gene mutation had a higher risk of AML progression, potentially providing a biomarker for progression. SIGNIFICANCE: Subclone expansion is a hallmark of progression from MDS to secondary AML. Subclonal signaling gene mutations are common at MDS (often at low levels), show complex and convergent patterns of clonal evolution, and are associated with future progression to secondary AML. See related article by Guess et al., p. 316 (33). See related commentary by Romine and van Galen, p. 270. This article is highlighted in the In This Issue feature, p. 265.
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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.