ReviewMolecular cancer2025
Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.
Review in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- KDM4B Maintains Pyruvate Dehydrogenase Complex Expression to Support Mitochondrial Metabolism and Survival in Cancer Cells.Epigenomes · 2026Article
- Development of a prognostic prediction model incorporatingJournal of gastrointestinal oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Breast cancer is a highly heterogeneous disease characterized by diverse molecular subtypes and complex pathogenesis. Recent advances in epigenetics have unveiled the crucial roles of lysine demethylases (KDMs) in modulating gene expression and chromatin dynamics, thereby influencing breast cancer progression, including metastasis, and therapeutic resistance. KDMs, which remove methyl groups from histone lysine residues, are mainly categorized into seven subfamilies (KDM1-7) based on their catalytic mechanisms and substrate specificities. Meanwhile, each subfamily exhibits distinct roles in breast cancer, ranging from transcriptional regulation and chromatin remodeling to interactions with non-histone proteins. Notably, KDMs exhibit subtype-specific functions in breast cancer. KDMs are also implicated in various hallmarks of breast cancer, including DNA damage response, cell cycle regulation, stemness maintenance, metabolic reprogramming, and modulation of the tumor microenvironment. KDMs represent promising targets for overcoming therapeutic resistance in breast cancer. Inhibitors targeting KDMs have shown potential to enhance the efficacy of endocrine therapy, chemotherapy, and targeted therapy by modulating oncogenic signaling pathways. The KDM family members are intricately involved in the molecular pathogenesis of breast cancer, offering a rich landscape for therapeutic intervention. This review summarizes the multifaceted molecular mechanisms and biological functions of KDMs in breast cancer, highlighting their potential as therapeutic targets.
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What Socratic 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 Socratic graph.