Mutational synergy during leukemia induction remodels chromatin accessibility, histone modifications and three-dimensional DNA topology to alter gene expression.

doi:10.1038/s41588-021-00925-9

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Mutational synergy during leukemia induction remodels chromatin accessibility, histone modifications and three-dimensional DNA topology to alter gene expression.

Nature genetics - 1 Oct 2021

Yun Haiyang, Narayan Nisha, Vohra Shabana, Giotopoulos George, Mupo Annalisa, Madrigal Pedro, Sasca Daniel, Lara-Astiaso David, Horton Sarah J, Agrawal-Singh Shuchi, Meduri Eshwar, Basheer Faisal, Marando Ludovica, Gozdecka Malgorzata, Dovey Oliver M, Castillo-Venzor Aracely, Wang Xiaonan, Gallipoli Paolo, Müller-Tidow Carsten, Osborne Cameron S, Vassiliou George S, Huntly Brian J P

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chromatin Assembly and Disassembly

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Enhancer Elements, Genetic

Share to fms-Like Tyrosine Kinase 3

Share to Gene Expression Regulation, Leukemic

Share to Gene Regulatory Networks

Share to Nucleophosmin

Share to Principal Component Analysis

Share to Protein Processing, Post-Translational

Source

Open in PubMed Open full text

Identifiers

PMID: 34556857
DOI: 10.1038/s41588-021-00925-9
PMCID: PMC7611829

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mutational synergy during leukemia induction remodels chromatin accessibility, histone modifications and three-dimensional DNA topology to alter gene expression.PMID 34556857Read ↗

Mutations Synergize to Alter Epigenetic and Genomic Landscape of AML.Semantic proximity Read ↗

Molecular pathogenesis of AML: translating insights to the clinic.Semantic proximity Read ↗

A distinct core regulatory module enforces oncogene expression in KMT2A-rearranged leukemiaSemantic proximity Read ↗

The genomic and epigenomic landscapes of AML.Semantic proximity Read ↗

Activating mutations remodel the chromatin accessibility landscape to drive distinct regulatory networks in KMT2A‐rearranged acute leukemiaSemantic proximity Read ↗

Transcriptional networks in acute myeloid leukemiaSemantic proximity Read ↗

Molecular synergy underlies the co-occurrence patterns and phenotype of NPM1-mutant acute myeloid leukemia.Semantic proximity Read ↗

Rewiring the Epigenetic Networks in MLL-Rearranged Leukemias: Epigenetic Dysregulation and Pharmacological InterventionsSemantic proximity Read ↗

New insights in AML biology from genomic analysis.Semantic proximity Read ↗

SETBP1 overexpression acts in the place of class-defining mutations to drive FLT3-ITD-mutant AML.Semantic proximity Read ↗

Chronic FLT3-ITD Signaling in Acute Myeloid Leukemia Is Connected to a Specific Chromatin Signature.Semantic proximity Read ↗

The transcriptomic landscape and directed chemical interrogation of MLL-rearranged acute myeloid leukemias.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.