ReviewMedComm2025
Colorectal Cancer: Pathogenesis and Targeted Therapy.
Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed.
- PRX5 as a critical driver of colorectal cancer stemness and tumorigenicity.Redox report : communications in free radical research · 2026Article
- RNF207 promotes colorectal cancer growth by regulating the Hippo-YAP pathway via enhanced MST1 ubiquitination and degradation.Journal of gastroenterology · 2026Article
- Targeting β-Adrenergic Signaling in Colorectal Cancer: Molecular Mechanisms and Therapeutic Potential of β-Blockers.Cancers · 2026Review
- Oral hydrogel systems in lower gastrointestinal disorders: From disease-based therapy to microbiota-guided design.Materials today. Bio · 2026Review
- Calcium hydroxide nanoparticles-induced oxidative stress and mitochondrial impairment drive genomic instability and programmed cell death in colorectal cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Epigallocatechin gallate enhances panobinostat-induced cytotoxicity through HDAC modulation in colorectal cancer cells.Molecular biology reports · 2026Article
- Automated model-based lesion tracking in CT: colorectal liver metastases as a use case for development and performance analysis.European radiology experimental · 2026Article
- EZH2 Regulates the Proliferation-Senescence Balance and Tumor-Stromal Signaling in Lung Adenocarcinoma.International journal of molecular sciences · 2026Article
- Phytochemistry, Bioavailability, and Molecular Mechanisms Underlying Multitarget Anticancer Activity ofNutrients · 2026Review
- Andean Berry (Molecules (Basel, Switzerland) · 2026Article
- Advanced drug delivery platforms targeting cellular senescence: A promising strategy for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- The Effect of Anti-Inflammatory Drugs on the Incidence of Colorectal Cancer.Pharmaceutics · 2026Review
- Microbiomics: Novel Biomarkers of Colorectal Cancer Diagnosis and Prognosis.Diagnostics (Basel, Switzerland) · 2026Review
- Lactate metabolism and lactylation in cancer: from pathogenesis to therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Colorectal cancer pathogenesis, oncogenic signaling networks and targeted therapeutic advances.Molecular biomedicine · 2026Review
- An automated image analysis pipeline for wide-field optical redox imaging of patient-derived cancer organoids.Scientific reports · 2026Article
- Glutamine-driven upregulation of NPDC1 promotes colorectal cancer progression through PI3K/AKT signaling.Journal of translational medicine · 2026Article
- The gut microbiome in colorectal cancer: mechanisms of carcinogenesis and emerging microbiota-targeted therapies.Discover oncology · 2026Review
- Gut microbiota-innate immune crosstalk in the initiation and progression of CRC: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- HIT101308137 and HIT104293658 nominate dual target chemotypes for PTPN1 and PTPN2 with preliminary selectivity in colorectal cancer cells.Frontiers in chemistry · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) ranks among the most prevalent malignant neoplasms globally. A growing body of evidence underscores the pivotal roles of genetic alterations and dysregulated epigenetic modifications in the pathogenesis of CRC. In recent years, the reprogramming of tumor cell metabolism has been increasingly acknowledged as a hallmark of cancer. Substantial evidence suggests a crosstalk between tumor cell metabolic reprogramming and epigenetic modifications, highlighting a complex interplay between metabolism and the epigenetic genome that warrants further investigation. Biomarkers associated with the pathogenesis and metabolic characteristics of CRC hold significant clinical implications. Nevertheless, elucidating the genetic, epigenetic, and metabolic landscapes of CRC continues to pose considerable challenges. Here, we attempt to summarize the key genes driving the onset and progression of CRC and the related epigenetic regulators, clarify the roles of gene expression and signaling pathways in tumor metabolism regulation, and explore the potential crosstalk between epigenetic events and tumor metabolic reprogramming, providing a comprehensive mechanistic explanation for the malignant progression of CRC. Finally, by integrating reliable targets from genetics, epigenetics, and metabolic processes that hold promise for translation into clinical practice, we aim to offer more strategies to overcome the bottlenecks in CRC treatment.
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Identifiers
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.