ArticleNature genetics2021
Mutational synergy during leukemia induction remodels chromatin accessibility, histone modifications and three-dimensional DNA topology to alter gene expression.
Article in Nature genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Inhibition of p300/CREBBP catalytic activity drives context-dependent transcriptional activation in AML.Blood · 2026Article
- Mutation Patterns Define Clinical Heterogeneity in Acute Myeloid Leukemia.Journal of Cancer · 2026Article
- Deciphering Haplotype-level Chromosome Conformation Alteration in Down Syndrome by Haplotype-resolved Multi-omics Analysis.Genomics, proteomics & bioinformatics · 2025Article
- Enforcement of stem-cell dormancy by nucleophosmin mutation is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis.Haematologica · 2025Article
- Regulation of H3K4me3 breadth and MYC expression by the SETD1B catalytic domain in MLL-rearranged leukemia.Leukemia · 2025Article
- Acute resistance to BET inhibitors remodels compensatory transcriptional programs via p300 coactivation.Blood · 2025Article
- Activating mutations remodel the chromatin accessibility landscape to drive distinct regulatory networks inHemaSphere · 2024Article
- Baf155 controls hematopoietic differentiation and regeneration through chromatin priming.Cell reports · 2024Article
- The landscape of RNA-chromatin interaction reveals small non-coding RNAs as essential mediators of leukemia maintenance.Leukemia · 2024Article
- Cre recombinase promotes leukemogenesis in the presence of both homozygous and heterozygous FLT3-ITD.Leukemia · 2024Article
- Cross-Species Comparative DNA Methylation Reveals Novel Insights into Complex Trait Genetics among Cattle, Sheep, and Goats.Molecular biology and evolution · 2024Article
- A new genomic framework to categorize pediatric acute myeloid leukemia.Nature genetics · 2024Article
- In vivo screening characterizes chromatin factor functions during normal and malignant hematopoiesis.Nature genetics · 2023Article
- The Molecular Context of Oxidant Stress Response in Cancer Establishes ALDH1A1 as a Critical Target: What This Means for Acute Myeloid Leukemia.International journal of molecular sciences · 2023Review
- Loop stacking organizes genome folding from TADs to chromosomes.Molecular cell · 2023Article
- Article
- Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia.Cancer discovery · 2023Article
- A novel network pharmacology approach for leukaemia differentiation therapy using MogrifyOncogene · 2022Article
- Dissection of the MEF2D-IRF8 transcriptional circuit dependency in acute myeloid leukemia.iScience · 2022Article
- PU.1-Dependent Enhancer Inhibition Separates Tet2-Deficient Hematopoiesis from Malignant Transformation.Blood cancer discovery · 2022Article
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
Abstract
Altered transcription is a cardinal feature of acute myeloid leukemia (AML); however, exactly how mutations synergize to remodel the epigenetic landscape and rewire three-dimensional DNA topology is unknown. Here, we apply an integrated genomic approach to a murine allelic series that models the two most common mutations in AML: Flt3-ITD and Npm1c. We then deconvolute the contribution of each mutation to alterations of the epigenetic landscape and genome organization, and infer how mutations synergize in the induction of AML. Our studies demonstrate that Flt3-ITD signals to chromatin to alter the epigenetic environment and synergizes with mutations in Npm1c to alter gene expression and drive leukemia induction. These analyses also allow the identification of long-range cis-regulatory circuits, including a previously unknown superenhancer of Hoxa locus, as well as larger and more detailed gene-regulatory networks, driven by transcription factors including PU.1 and IRF8, whose importance we demonstrate through perturbation of network members.
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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 Socratic graph.