ReviewMolecular oncology2012
Chromatin remodeling in cancer: a gateway to regulate gene transcription.
Review in Molecular oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed.
- Chromatin regulator expression patterns predict prognosis and guide neoadjuvant therapy in esophageal squamous cell carcinoma.Fundamental research · 2026Article
- Phenolic compounds and chemotherapeutic agents differentially regulate P2X receptor subtypes in malignant melanoma.Purinergic signalling · 2026Article
- Neuroendocrine-associated epigenetic factors in cellular senescence: mechanisms and therapeutic implications.Biogerontology · 2026Review
- Cooperative and Opposing Functions of ANP32E and VPS72 Govern Gene Promoter Chromatin Status.Research square · 2026Article
- Integrative phosphoproteomic analysis identifies functional roles of TRPM7 phosphosites in oncogenesis.Frontiers in bioinformatics · 2026Article
- Selisistat, a SIRT1 inhibitor, enhances paclitaxel activity in luminal and triple-negative breast cancer: in silico, in vitro, and in vivo studies.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Comprehensive Pan-Cancer Analysis of ZNF668 Reveals the Prognostic and Immunological Significance of ZNF668.Current issues in molecular biology · 2025Article
- Missense mutations in intrinsically disordered protein regions link pathogenicity and phase separation.The Journal of biological chemistry · 2025Article
- LncRNA CASC19 promotes pancreatic cancer progression by increasing PSPC1 protein stability and facilitating the oncogenic PSPC1/ β-Catenin pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Transforming Cancer Diagnostics: The Emergence of Liquid Biopsy and Epigenetic Markers.MedComm · 2025Review
- Epigenetic modifiers to enhance the efficacy of immune checkpoint inhibitors for the treatment of melanoma.Translational oncology · 2025Review
- Epigenetic Modulation and Bone Metastasis: Evolving Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Covalent adduct Grob fragmentation underlies LSD1 demethylase-specific inhibitor mechanism of action and resistance.Nature communications · 2025Article
- Combining Quantitative Proteomics and Interactomics for a Deeper Insight into Molecular Differences between Human Cell Lines.Journal of proteome research · 2024Article
- The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024Review
- Combining quantitative proteomics and interactomics for a deeper insight into molecular differences between human cell lines.bioRxiv : the preprint server for biology · 2024Article
- Cellular and clinical impact of protein phosphatase enzyme epigenetic silencing in multiple cancer tissues.Human genomics · 2024Article
- Involvement of CCCTC-binding factor in epigenetic regulation of cancer.Molecular biology reports · 2023Review
- The integrative multi-omics approach identifies the novel competing endogenous RNA (ceRNA) network in colorectal cancer.Scientific reports · 2023Article
- Novel Insights into the Role of Chromatin Remodeler MORC2 in Cancer.Biomolecules · 2023Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Cancer cells are remarkably adaptive to diverse survival strategies, probably due to its ability to interpret signaling cues differently than the normal cells. It appears as if cancer cells are constantly sampling, selecting and adapting signaling pathways to favor its proliferation. This process of successful adaptive evolution eventually renders a retractile nature to therapeutic regimens, fueling to the process of cancer progression. Based on plethora of available information, it is now evident that multiple signaling pathways eventually converge, perhaps, in a tempo-spatial manner, onto DNA template-dependent dynamic processes. Considering the complexity and packaging of eukaryotic genome, this process involves energy-dependent sub-events mediated by chromatin remodelers. Chromatin remodeler proteins function as gatekeepers and constitute a major determinant of accessibility of accessory factors to nucleosome DNA, allowing a wide repertoire of biological functions. And thus, aberrant expression or epigenetic modulation of remodeler proteins confers a unique ability to cancer cells to reprogram its genome for the maintenance of oncogenic phenotypes. Cancer cells can uniquely select a multi-subunit remodeler proteome for oncogenic advantage. This review summarizes our current understanding and importance of remodeler and chromatin proteins in cancer biology and also highlights the paradoxical role of proteins with or without dual-regulator functions. It is our hope that an in-depth understanding of these events is likely to provide a next set of opportunities for novel strategies for targeted cancer therapeutics.
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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.