ArticleJournal of gastrointestinal cancer2023
To β or Not to β: Lack of Correlation Between APC Mutation and β-Catenin Nuclear Localization in Colorectal Cancer.
Article in Journal of gastrointestinal cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- KRT80 promotes colon adenocarcinoma progression via stat3 pathway activation and immune microenvironment remodeling.Translational cancer research · 2026Article
- RNA-binding protein RBM47 in health and disease: molecular mechanisms, preclinical evidence, and translational challenges.Frontiers in immunology · 2026Review
- Cytoplasmic TRIM24 promotes colorectal cancer cell proliferation by activating Wnt/β-catenin signaling.Nature communications · 2025Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeColorectal cancer (CRC) appears to arise from sequential genetic lesions in tumor suppressor genes (APC, SMAD4, and TP53) and oncogenes (KRAS) leading to the classical adenoma to carcinoma progression. Biallelic APC inactivating genetic aberrations are detected in about 70% of early microadenomas implicating APC inactivation as the first genetic hit in CRC. APC is an essential protein of the Wnt 'destruction complex'; APC inactivation is believed to cause disruption of the complex allowing stabilization and nuclear translocation of β-catenin, resulting in transcriptional activation of cancer-promoting genes.
methodsβ-catenin nuclear localization and APC mutation were validated from serial FFPE sections representing the same tumor regions, using immunohistochemistry and Sanger sequencing, respectively.
resultsHere, we provide evidence for a surprising lack of correlation between APC mutation and β-catenin nuclear localization in early-onset sporadic rectal cancer samples. Several factors including status of KRAS mutation could not explain this anomaly. The lack of correlation was validated in CRC cell lines harboring various APC mutations.
conclusionOur results provide evidence directly from tumor samples for possible non-canonical role(s) for mutant APC.
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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.