ArticleCancer medicine2025
Focal Adhesion Kinase Intersects With the BRD4-MYC Axis and YAP1 to Drive Tumor Cell Growth, Phenotypic Plasticity, Stemness, and Metastatic Potential in Colorectal Cancer.
Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Plasma miRNA-Metabolite Dysregulation in People with HIV with Cirrhosis Despite Successful HCV Cure.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Dual targeting of oncogenic microtubules and mitochondria in PDAC.Oncoscience · 2026Article
- Focal Adhesion Kinase Intersects With the BRD4-MYC Axis and YAP1 to Drive Tumor Cell Growth, Phenotypic Plasticity, Stemness, and Metastatic Potential in Colorectal Cancer.Cancer medicine · 2025Article
- Integrin alpha L: structure, cellular functions, and emerging role in human diseases.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors.
Funding
Abstract
objectiveColorectal cancer (CRC) remains one of the leading causes of cancer-related death worldwide due to the lack of effective therapies. Here we explored the clinical basis and therapeutic promise of the integrin-focal adhesion kinase (FAK)-dependent pathway for CRC. METHODS AND
resultsOur bioinformatic and histological analyses showed that FAK was markedly upregulated at both mRNA and protein and signaling levels in the two CRC patient cohorts. Particularly, the portion of carcinomas carrying active FAK (Y
conclusionOverall, our study highlights the potent pro-malignant role of the integrin-FAK axis in CRC, fueling its targeting as a single agent or synthetic lethal-based therapy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.