ReviewCells2020
Methylation-Based Therapies for Colorectal Cancer.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Distant Metastasis in Colorectal Cancer Patients-Do We Have New Predicting Clinicopathological and Molecular Biomarkers? A Comprehensive Review.International journal of molecular sciences · 2020Pooled it
- Transcription Activation of DEPDC1B Upon EBF1 Loss Contributes to Cell Cycle Progression and Epithelial-Mesenchymal Transition in Colon Adenocarcinoma.Biochemical genetics · 2026Article
- The Role of Next-Generation Probiotics in Colorectal Cancer Pathways: Mechanisms and Therapeutic Potential.Probiotics and antimicrobial proteins · 2026Review
- Epigenetic Alterations in Colitis-Associated Colorectal Cancer.Epigenomes · 2026Review
- Development of an application for colorectal cancer prediction using SDC2 and TFPI2 methylation: an opportunity for early and noninvasive diagnosis in Latin-America.Frontiers in molecular biosciences · 2026Article
- Gain of function p53 mutant R273H confers distinct methylation profiles and consequent YAP/TAZ signaling mediated activation of partial or full EMT states to colon tumours.Epigenetics & chromatin · 2025Article
- Non-invasive colorectal cancer screening methods: focusing on diagnostic genetic and epigenetic markers.Cancer cell international · 2025Review
- Targeting epigenetic modifications as an emerging immunotherapeutic strategy for cancers.Immunologic research · 2025Review
- Integrating gene demethylation and immune modulation: PD-1 nanovesicles as a dual-action therapy for NSCLC.Materials today. Bio · 2025Article
- Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer.International journal of molecular sciences · 2025Review
- DNA methylation biomarkers for predicting lymph node metastasis in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- The value of SDC2 and Septin9 combined with serum tumor markers in early diagnosis of colorectal cancer.International journal of colorectal disease · 2024Article
- The up-regulation of SYNCRIP promotes the proliferation and tumorigenesis via DNMT3A/p16 in colorectal cancer.Scientific reports · 2024Article
- DNA hypomethylation patterns and their impact on the tumor microenvironment in colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- The epigenetic landscape in intestinal stem cells and its deregulation in colorectal cancer.Stem cells (Dayton, Ohio) · 2024Review
- NLRC5 promotes endometrial carcinoma progression by regulating NF-κB pathway-mediated mismatch repair gene deficiency.Scientific reports · 2024Article
- Comprehensive RNA-sequencing analysis of colorectal cancer in a Korean cohort.Molecules and cells · 2024Article
- DNA Methylation Signatures of Response to Conventional Synthetic and Biologic Disease-Modifying Antirheumatic Drugs (DMARDs) in Rheumatoid Arthritis.Biomedicines · 2023Review
- Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal carcinogenesis (CRC) is caused by the gradual long-term accumulation of both genetic and epigenetic changes. Recently, epigenetic alterations have been included in the classification of the CRC molecular subtype, and this points out their prognostic impact. As epigenetic modifications are reversible, they may represent relevant therapeutic targets. DNA methylation, catalyzed by DNA methyltransferases (DNMTs), regulates gene expression. For many years, the deregulation of DNA methylation has been considered to play a substantial part in CRC etiology and evolution. Despite considerable advances in CRC treatment, patient therapy response persists as limited, and their profit from systemic therapies are often hampered by the introduction of chemoresistance. In addition, inter-individual changes in therapy response in CRC patients can arise from their specific (epi)genetic compositions. In this review article, we summarize the options of CRC treatment based on DNA methylation status for their predictive value. This review also includes the therapy outcomes based on the patient's methylation status in CRC patients. In addition, the current challenge of research is to develop therapeutic inhibitors of DNMT. Based on the essential role of DNA methylation in CRC development, the application of DNMT inhibitors was recently proposed for the treatment of CRC patients, especially in patients with DNA hypermethylation.
Indexed as
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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.