ArticleCell stem cell2017
Human AML-iPSCs Reacquire Leukemic Properties after Differentiation and Model Clonal Variation of Disease.
Article in Cell stem cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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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.
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Who cites it
79 citing papers in PubMed, 127 citations in OpenAlex.
- Targeting IMPDH to inhibit SAMHD1 inCell cycle (Georgetown, Tex.) · 2026Article
- Human iPSC-derived and conventional cancer models in precision oncology: advancing patient-specific therapies from bench to bedside.Journal of experimental & clinical cancer research : CR · 2026Review
- DNMT3A R882H Is Not Required for Disease Maintenance in Primary Human AML but Is Associated with Increased Leukemia Stem Cell Frequency.Cancer discovery · 2026Article
- Article
- Targeting dysregulated epigenetic and transcription factor networks inBlood neoplasia · 2026Article
- Modeling myeloid cell development in health and disease using induced pluripotent stem cells.Frontiers in immunology · 2026Review
- VHL Gene Restoration Supports RCC Reprogramming to iPSCs but Does Not Ensure Line Stability.Cancers · 2025Article
- SF3B1-mutant models of RNA mis-splicing uncover UBA1 as a therapeutic target in myelodysplastic neoplasms.Leukemia · 2025Article
- iPSC-derived MSCs alleviate arthritis in collagen-induced arthritis mice by reducing synovial CD86h iIL1βhi macrophage.Stem cells translational medicine · 2025Article
- Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025Review
- Human iPSC-based breast cancer model identifies S100P-dependent cancer stemness induced byScience advances · 2025Article
- Protocol for the generation of HLF+ HOXA+ human hematopoietic progenitor cells from pluripotent stem cells.STAR protocols · 2025Article
- The Crossroads of Clonal Evolution, Differentiation Hierarchy, and Ontogeny in Leukemia Development.Blood cancer discovery · 2025Review
- Understanding Human Oncogene Function and Cooperativity in Myeloid Malignancy Using iPSCs.Experimental hematology · 2025Review
- Examining patient-specific responses to PARP inhibitors in a novel, human induced pluripotent stem cell-based model of breast cancer.NPJ precision oncology · 2025Article
- Genome engineering with Cas9 and AAV repair templates generates frequent concatemeric insertions of viral vectors.Nature biotechnology · 2025Article
- Lineage-tracing hematopoietic stem cell origins in vivo to efficiently make human HLF+ HOXA+ hematopoietic progenitors from pluripotent stem cells.Developmental cell · 2024Article
- Monoallelic KRAS (G13C) mutation triggers dysregulated expansion in induced pluripotent stem cell-derived hematopoietic progenitor cells.Stem cell research & therapy · 2024Article
- Evaluation of the safety and efficiency of cytotoxic T cell therapy sensitized by tumor antigens original from T-ALL-iPSC in vivo.Cancer innovation · 2024Article
- Review
19 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Understanding the relative contributions of genetic and epigenetic abnormalities to acute myeloid leukemia (AML) should assist integrated design of targeted therapies. In this study, we generated induced pluripotent stem cells (iPSCs) from AML patient samples harboring MLL rearrangements and found that they retained leukemic mutations but reset leukemic DNA methylation/gene expression patterns. AML-iPSCs lacked leukemic potential, but when differentiated into hematopoietic cells, they reacquired the ability to give rise to leukemia in vivo and reestablished leukemic DNA methylation/gene expression patterns, including an aberrant MLL signature. Epigenetic reprogramming was therefore not sufficient to eliminate leukemic behavior. This approach also allowed us to study the properties of distinct AML subclones, including differential drug susceptibilities of KRAS mutant and wild-type cells, and predict relapse based on increased cytarabine resistance of a KRAS wild-type subclone. Overall, our findings illustrate the value of AML-iPSCs for investigating the mechanistic basis and clonal properties of human AML.
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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.