ReviewOncology letters2025
Mechanism of APC truncation involved in colorectal cancer tumorigenesis (Review).
Review in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Colorectal cancer sidedness: prognostic implications and the predictive role of artificial intelligence.BMC medical informatics and decision making · 2026Article
- Multi Omics Integration in Colorectal Cancer: From Molecular Insights to Precision Oncology.Cancers · 2026Review
- TruncatingJournal of cancer prevention · 2026Article
- Evaluation of Activated Biochar Derived fromBiosensors · 2026Article
- Colorectal cancer liver metastasis: immunosuppressive microenvironment, signaling pathways, and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- Case Report: Occult mantle cell lymphoma in a synchronous rectal collision tumor with adenocarcinoma: retrospective reclassification and multispecimen molecular profiling.Frontiers in oncology · 2026Article
- Common oncogenic mutations in colorectal cancer: drivers of carcinogenesis and potential therapeutic targets.Frontiers in pharmacology · 2026Review
- Genetic, Epidemiological, Clinical, and Therapeutic Trajectories in Colon and Rectal Cancers.Cancers · 2025Review
- WNT signaling in cancer: molecular mechanisms and potential therapies.Molecular biomedicine · 2025Review
- The Anti-Inflammatory, Immunomodulatory, and Pro-Autophagy Activities of Probiotics for Colorectal Cancer Prevention and Treatment: A Narrative Review.Biomedicines · 2025Review
- Signature Gene Mutations in Colorectal Cancer: Potential Neoantigens for Cancer Vaccines.International journal of molecular sciences · 2025Review
- RNA-based therapies for colorectal cancer: targeting the β-catenin pathway via microbiota -modulated miRNAs.Frontiers in molecular biosciences · 2025Review
- Assessment of the relationship between gut microbiota, inflammatory markers, and colorectal cancer.Frontiers in cellular and infection microbiology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenomatous polyposis coli (APC) is widely recognized as a heavily mutated gene that suppresses tumor growth in colorectal cancer (CRC). Its mutation is considered to be the primary and early event that occurs in the development of CRC. In addition, APC has a crucial role in inhibiting the canonical Wnt signaling pathway. APC mutations in CRC result in the production of shortened gene products. This impairment of β-catenin destruction complexes causes an accumulation of active β-catenin in the cytoplasm and nucleus. In these compartments, β-catenin can bind with DNA-binding proteins of the transcription factor/lymphoid enhancer-binding factor family, thereby activating the Wnt signaling pathway. Consequently, the balance of numerous cellular processes is disrupted, ultimately driving the formation of tumors. There is a growing body of evidence indicating the prevalent occurrence of APC truncation in the majority of CRC cases. Furthermore, it has been observed that these truncated proteins have a crucial role in the activation of the Wnt signaling pathway and the subsequent loss of tumor inhibitory function. This review aimed to provide an overview of the recent advancements in understanding the mechanism behind APC truncation and its association with the onset and progression of CRC.
Indexed as
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.