ReviewGenes2025
Chromatin Remodulator CHD4: A Potential Target for Cancer Interception.
Review in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Role of CHD4 in tumor progression, DNA damage response and treatment resistance (Review).Oncology reports · 2026Review
- ELK3 promotes cisplatin resistance in ovarian cancer via regulating CHD4 gene expression.Discover oncology · 2026Article
- CHD4 epigenetically coordinates genomic instability and immunosuppression to drive pan-cancer progression and confer HDAC inhibitor sensitivity.Clinical and experimental medicine · 2026Article
- IKAROS Gene Regulatory Network Reveal ERG as a Vulnerability in B-cell Acute Lymphoblastic Leukemia.bioRxiv : the preprint server for biology · 2025Article
- CHD1 dysregulation in cancer: bridging chromatin instability, therapy resistance, and immune evasion.Molecular biology reports · 2025Review
- Case Report: Novel mutation in CHD4 triggers occult breast cancer with bone metastases.Frontiers in oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cancer initiation and progression are associated with numerous somatic mutations, genomic rearrangements, and structure variants. The transformation of a normal cell into a cancer cell involves spatio-temporal changes in the regulation of different gene networks. The accessibility of these genes within the cell nucleus is manipulated via nucleosome remodeling ATPases, comprising one of the important mechanisms. Here, we reviewed studies of an ATP-dependent chromatin remodulator, chromodomain helicase DNA-binding 4 (CHD4), in cancer. Multiple domains of CHD4 are known to take part in nucleosome mobilization and histone binding. By binding with other proteins, CHD4 plays a vital role in transcriptional reprogramming and functions as a key component of Nucleosome Remodeling and Deacetylase, or NuRD, complexes. Here, we revisit data that demonstrate the role of CHD4 in cancer progression, tumor cell proliferation, DNA damage responses, and immune modulation. Conclusively, CHD4-mediated chromatin accessibility is essential for transcriptional reprogramming, which in turn is associated with tumor cell proliferation and cancer development.
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What OpenQuestion holds
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.