Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Acute myeloid leukemia (AML) is a heterogeneous disease caused by mutations in transcriptional regulator genes, but how different mutant regulators shape the chromatin landscape is unclear. Here, we compared the transcriptional networks of two types of AML with chromosomal translocations of the RUNX1 locus that fuse the RUNX1 DNA-binding domain to different regulators, the t(8;21) expressing RUNX1-ETO and the t(3;21) expressing RUNX1-EVI1. Despite containing the same DNA-binding domain, the two fusion proteins display distinct binding patterns, show differences in gene expression and chromatin landscape, and are dependent on different transcription factors. RUNX1-EVI1 directs a stem cell-like transcriptional network reliant on GATA2, whereas that of RUNX1-ETO-expressing cells is more mature and depends on RUNX1. However, both types of AML are dependent on the continuous expression of the fusion proteins. Our data provide a molecular explanation for the differences in clinical prognosis for these types of AML.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5457485 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2017.05.005 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Epigenetic regulation and maternal-to-zygotic transition in dwarf surf clam ( ): Insights from chromatin state profiling and transcriptomics.
Zool Res
September 2025
MOE Key Laboratory of Marine Genetics and Breeding, College of Marine Life Sciences, Ocean University of China, Qingdao, Shandong 266003, China.
Bivalve mollusks represent a taxonomically and economically significant clade within Mollusca. However, the regulatory mechanisms governing their embryonic development remain poorly characterized. The dwarf surf clam ( ), characterized by a short generation time and high fecundity, has recently gained recognition as an ideal model system for bivalve embryological research.
View Article and Find Full Text PDFAging-associated DNA methylation of LEF1 modulates inflammation and neurodegenerative pathways.
Front Immunol
September 2025
Department of Blood Transfusion, Huashan Hospital, Fudan University, Shanghai, China.
Background: Aging is accompanied by profound changes in immune regulation and epigenetic landscapes, yet the molecular drivers underlying these alterations are not fully understood.
Methods: Transcriptional profiles of peripheral blood samples from young and elderly individuals, together with aging-associated methylation probe data, were used to identify aging biomarkers. Transcriptomics and chromatin immunoprecipitation sequencing (ChIP-Seq) were conducted to explore potential regulatory mechanisms.
A high-resolution meiotic crossover map from single-nucleus ATAC-seq reveals insights into the recombination landscape in mammals.
NAR Genom Bioinform
September 2025
DNA Repair and Recombination Laboratory, St Vincent's Institute of Medical Research, Fitzroy VIC 3065, Australia.
Meiotic crossovers promote correct chromosome segregation and the shuffling of genetic diversity. However, the measurement of crossovers remains challenging, impeding our ability to decipher the molecular mechanisms that are necessary for their formation and regulation. Here we demonstrate a novel repurposing of the single-nucleus Assay for Transposase Accessible Chromatin with sequencing (snATAC-seq) as a simple and high-throughput method to identify and characterize meiotic crossovers from haploid testis nuclei.
View Article and Find Full Text PDFATPase-deficient CHD7 disease variant disrupts neural development via chromatin dysregulation.
J Genet Genomics
September 2025
Institute of Pediatrics, Children's Hospital of Fudan University, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China; Sh
Chromodomain helicase DNA binding protein 7 (CHD7), an ATP-dependent chromatin remodeler, plays versatile roles in neurodevelopment. However, the functional significance of its ATPase/nucleosome remodeling activity remains incompletely understood. Here, we generate genetically engineered mouse embryonic stem cell lines harboring either an inducible Chd7 knockout or an ATPase-deficient missense variant identified in individuals with CHD7-related disorders.
View Article and Find Full Text PDFComprehensive analysis of oncogenic determinants across tumor types via multi-omics integration.
Cancer Genet
August 2025
National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, India. Electronic address:
Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic and epigenetic alterations that drive uncontrolled cellular proliferation and survival. This review provides a comprehensive overview of key cancer driver genes, including oncogenes such as KRAS and PIK3CA, as well as tumor suppressor genes like TP53, PTEN, and CDKN2A, highlighting their molecular mechanisms and roles across various types of cancer. Leveraging insights from large-scale cancer genome initiatives and whole-genome sequencing, we examine the landscape of somatic mutations and their association with hallmark cancer pathways, including cell cycle regulation, apoptosis, metabolic reprogramming, and immune evasion.
View Article and Find Full Text PDF