ArticleWorld journal of gastrointestinal oncology2025
Article in World journal of gastrointestinal oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Colitis-Associated Colorectal Cancer-STAT3 Inhibition as a Preventive Strategy.International journal of molecular sciences · 2026Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is the second leading cause of cancer-related death, largely due to limited treatment options in advanced stages. Genomic alterations in advanced CRC (aCRC) are complex and not fully characterized, with only 30% of patients benefiting from targeted therapies.
aimTo investigate the molecular heterogeneity of primary aCRC in order to identify clinically relevant genomic alterations.
methodsWe conducted a retrospective molecular analysis of 73 consecutive patients with histologically confirmed primary aCRC (stage pT4a-b). All molecular findings were correlated with available clinicopathological data. In addition, we performed survival analyses using publicly available datasets and tools.
resultsGenetic abnormalities identified in primary tumors were most frequently mutations in tumor protein p53 (58% of cases), Kirsten rat sarcoma viral oncogene homolog (52%), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (25%), B-Raf kinase (11%) and fibroblast growth factor receptor 3 (8%), as well as R-spondin 3 (
conclusionThis study identifies a relatively high incidence of
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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.