ArticleCancers2020
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 47 citations in OpenAlex.
- GNG12 overexpression inhibits triple-negative breast cancer cell proliferation, migration, and invasion.Scientific reports · 2026Article
- Impact of non-genetic heterogeneity of BRAF-mutant colon cancer organoids on growth kinetics, drug sensitivity and Wnt dynamics.International journal of cancer · 2026Article
- The Mechanistic Crosstalk between Probiotics, ncRNAs, and Autophagy: Implications for Colorectal Cancer Precision Medicine.Expert reviews in molecular medicine · 2026Review
- Attenuation of the CpG island methylator phenotype and lack of WNT signalling activation restrains Kras mutant intestinal neoplasia.British journal of cancer · 2026Article
- Novel Syngeneic Cell Lines for Studying High-Risk BRAFV600E-Driven Colorectal Cancer In Vivo.Cancer research communications · 2026Article
- Common gene mutations in 103 authenticated colorectal cancer cell lines.Oncogenesis · 2026Article
- BRAF mutation and tumor immune microenvironment in new era.American journal of cancer research · 2026Review
- Colorectal Cancer Progression and Bone Metastasis: Molecular Mechanisms, Tumor Microenvironment, and Tumor-Bone Crosstalk.Cancer management and research · 2026Review
- Integrated In Silico and Experimental Validation of Antrocin as a Plant-Derived Multi-Target Therapeutic for BRAF/MEK/PI3K-Driven Colorectal Cancer.International journal of molecular sciences · 2025Article
- Distinctive chromosomal, mutational and transcriptional profiling in colon versus rectal cancers.Journal of translational medicine · 2025Article
- Emerging Frontiers in Colorectal Cancer Therapy: From Targeted Molecules to Immunomodulatory Breakthroughs and Cell-Based Approaches.Digestive diseases and sciences · 2025Review
- Review
- Exploring WNT pathway dysregulation in serrated colorectal cancer for improved diagnostic and therapeutic strategies.Frontiers in genetics · 2025Article
- New insights in ubiquitin-dependent Wnt receptor regulation in tumorigenesis.In vitro cellular & developmental biology. Animal · 2024Review
- Pancreatic Neuroendocrine Tumors: Signaling Pathways and Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Clinical and molecular characteristics ofTherapeutic advances in medical oncology · 2024Article
- Leveraging a disulfidptosis‑related lncRNAs signature for predicting the prognosis and immunotherapy of glioma.Cancer cell international · 2023Article
- Clinical research progress on BRAF V600E-mutant advanced colorectal cancer.Journal of cancer research and clinical oncology · 2023Review
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Metastasising ameloblastoma or ameloblastic carcinoma? A case report with mutation analyses.BMC oral health · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWNT activation is a hallmark of colorectal cancer.
methodswe performed exome-sequencing on 24 BRAF mutant colorectal cancers and analyzed these data in combination with 175 publicly available BRAF mutant colorectal cancer exomes. We assessed the somatic mutational landscape of WNT signaling regulators, and performed hotspot and driver mutation analyses to identify potential drivers of WNT signaling. The effects of Apc and Braf mutation were modelled, in vivo, using the Apc
resultsRNF43 was the most frequently mutated WNT signaling regulator (41%). Mutations in the beta-catenin destruction complex occurred in 48% of cancers. Hotspot analyses identified potential cancer driver genes in the WNT signaling cascade, including MEN1, GNG12 and WNT16. Truncating APC mutation was identified in 20.8% of cancers. Truncating APC mutation was associated with early age at diagnosis (p < 2 × 10
conclusionsthe WNT signaling axis is frequently mutated in BRAF mutant colorectal cancers. WNT16 and MEN1 may be novel drivers of aberrant WNT signaling in colorectal cancer. Co-mutation of BRAF and APC generates an extremely aggressive neoplastic phenotype that is associated with poor patient outcome.
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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.