ReviewJournal of translational medicine2025
p53 in colorectal cancer: from a master player to a privileged therapy target.
Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed.
- An AI-integrated organoid platform enables high-throughput functional evaluation of bioactive metal ions.Bioactive materials · 2026Article
- High KPNA2 expression predicts poor prognosis in pathological T4 colorectal cancer by importing c-Myc into the nucleus to suppress p53-dependent p21 expression.British journal of cancer · 2026Article
- KRAS in Colorectal Cancer: Tumorigenesis, Surgical Implications and Evolving Treatment Target.Current oncology (Toronto, Ont.) · 2026Review
- Autophagy Orchestrates Anti-Tumor Immunity to Enhance Chemosensitivity via the FBXW2/C/EBPβ/TIMP-2 Axis in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SETD8-mediated mono-methylation of YAP at K76 promotes K48-linked polyubiquitination and degradation to suppress colorectal cancer.Cell death and differentiation · 2026Article
- Searching for Novel Molecular Prognostic Markers in Colorectal Cancer-The Tumor Suppressor Proteins p53 and PTEN.Biomedicines · 2026Article
- Molecular Profiling and Selective Pro-Apoptotic Activity of a Pruning-DerivedInternational journal of molecular sciences · 2026Article
- Molecular Characterization ofCancers · 2026Article
- Article
- Multi Omics Integration in Colorectal Cancer: From Molecular Insights to Precision Oncology.Cancers · 2026Review
- Targeting phase separation: a new strategy to disrupt the stromal-immune axis in colorectal cancer.Cell communication and signaling : CCS · 2026Review
- GDPD5-CD55-EGFR competitive binding axis regulates radioresistance and lipid accumulation in rectal cancer.Cell death & disease · 2026Article
- TP53 Loss Fuels mTORC1 Activation and Autophagy Suppression to Drive Immune-Cold Colorectal Cancer.World journal of oncology · 2026Article
- FBXO39 promotes LDHA-mediated aerobic glycolysis and colorectal cancer progression by p53 degradation.Journal of translational medicine · 2026Article
- Colorectal cancer pathogenesis, oncogenic signaling networks and targeted therapeutic advances.Molecular biomedicine · 2026Review
- Article
- Lactylation in cancer: molecular mechanisms and advances in clinical study.Molecular cancer · 2026Review
- Microbial metabolic profiling reshapes NF-κB-mediated immune metabolic network: a new mechanism for CRC development.Journal of translational medicine · 2026Review
- The differential effects of CBD and CBDA on viability and mRNA expression in colorectal cancer cells.Journal of cannabis research · 2026Article
- Nuclear-Cytoplasmic Axis in Cancer: From Protein Mislocalization to Anticancer Drug Resistance.Oncology research · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Colorectal cancer (CRC) is the third most prevalent malignancy and the second leading cause of cancer-related mortality worldwide. The pathogenesis of CRC primarily stems from the gradual accumulation of genetic mutations, which drive oncogene (e.g., KRAS) activation and tumor suppressor gene (e.g., TP53) inactivation. Loss of genetic stability facilitates the conversion of proto-oncogenes into active oncogenes and the functional impairment of tumor suppressors, collectively propelling CRC progression. The tumor suppressor protein p53, a transcription factor, induces cell cycle arrest, apoptosis, and DNA damage repair under cellular stress, and prevents cancer development by regulating various cellular responses. However, in CRC pathogenesis, TP53 mutations (detected in ~ 74% of cases) subvert these protective mechanisms through dual mechanisms: (i) dominant-negative suppression of wild-type p53 (wt-p53) function, and (ii) acquisition of neomorphic pro-tumorigenic activities, termed gain-of-function (GOF) mutations. New evidence from laboratory and clinical trials shows that some new therapeutic strategies have the potential to treat CRC by reactivating and restoring p53 function, depleting p53 mutants, or targeting p53 with immunotherapy. In this review, we summarize the function of p53 and characterize its mutation in CRC, emphasizing the influence of p53 mutation in the pathogenesis of CRC. In addition, we also describe the current therapeutic strategies for targeting p53 mutants in CRC.
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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.