ArticleNature medicine2022
Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy.
Article in Nature medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
What it found
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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
55 citing papers in PubMed, 80 citations in OpenAlex.
- Olutasidenib alone or combined with azacitidine in patients with mutant IDH1 myelodysplastic syndrome.Blood advances · 2025Trial
- Article
- Genomic Subtype Influences BH3 Mimetic Drug Sensitivity and Synergy with Cytotoxic Chemotherapeutics in T-cell Acute Lymphoblastic Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Initial leukemic epigenomic state determines hypomethylating agent response.Nature communications · 2026Article
- Article
- Impact of allogeneic stem cell transplantation in patients with higher risk myelodysplastic syndromes.Blood cancer journal · 2026Article
- Circular RNA expression landscapes in myelodysplastic neoplasms: Associations with mutational signatures and disease progression.Molecular oncology · 2026Article
- T lymphocytes and natural killer cells in myelodysplastic syndromes: function, dysfunction, and therapeutic potential.Frontiers in immunology · 2026Review
- Bone marrow microenvironment reprogramming in myelodysplastic neoplasms: from pathological mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Myelodysplastic syndrome progress to acute myeloid leukemia: new insights and updates.Frontiers in immunology · 2026Review
- Article
- Single-cell transcriptomic characterization of a human MDS hematopoietic dataset and in vitro validation of apoptosis-related venetoclax resistance in human MDS-L cells.Frontiers in cell and developmental biology · 2026Article
- Chromatin accessibility in stem cells unveils progressive transcriptional alterations in myelodysplastic syndrome.Nature communications · 2025Article
- A Brief Review on the Role of the Transcription Factor PBX1 in Hematologic Malignancies.International journal of molecular sciences · 2025Review
- Myelodysplastic syndromes: Updates on Genomic Landscape, Molecular Subtypes, & Targeted Therapies.Current hematologic malignancy reports · 2025Review
- Understanding infectious complications in patients with lower-risk myelodysplastic syndromes: a step towards improving survival.Haematologica · 2025Article
- Hematopoietic Stem Cell Hierarchies as Novel Biomarkers of Drug Response in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- TLR7/8 ligands R848 and imiquimod induce differentiation of bone marrow cells from patients with myelodysplastic syndrome towards mature neutrophils.Scientific reports · 2025Article
- Cell Marker Accordion: interpretable single-cell and spatial omics annotation in health and disease.Nature communications · 2025Article
- A reference model of circulating hematopoietic stem cells across the lifespan with applications to diagnostics.Nature medicine · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
38 authors at 5 institutions in 2 countries.
Funding
Abstract
Myelodysplastic syndromes (MDS) are heterogeneous neoplastic disorders of hematopoietic stem cells (HSCs). The current standard of care for patients with MDS is hypomethylating agent (HMA)-based therapy; however, almost 50% of MDS patients fail HMA therapy and progress to acute myeloid leukemia, facing a dismal prognosis due to lack of approved second-line treatment options. As cancer stem cells are the seeds of disease progression, we investigated the biological properties of the MDS HSCs that drive disease evolution, seeking to uncover vulnerabilities that could be therapeutically exploited. Through integrative molecular profiling of HSCs and progenitor cells in large patient cohorts, we found that MDS HSCs in two distinct differentiation states are maintained throughout the clinical course of the disease, and expand at progression, depending on recurrent activation of the anti-apoptotic regulator BCL-2 or nuclear factor-kappa B-mediated survival pathways. Pharmacologically inhibiting these pathways depleted MDS HSCs and reduced tumor burden in experimental systems. Further, patients with MDS who progressed after failure to frontline HMA therapy and whose HSCs upregulated BCL-2 achieved improved clinical responses to venetoclax-based therapy in the clinical setting. Overall, our study uncovers that HSC architectures in MDS are potential predictive biomarkers to guide second-line treatments after HMA failure. These findings warrant further investigation of HSC-specific survival pathways to identify new therapeutic targets of clinical potential in MDS.
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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.