ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
ETV4 Promotes Colorectal Cancer Progression by Reprogramming Asparagine Metabolism to Remodel the Stromal Microenvironment.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. 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
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
2 citing papers in PubMed.
- Article
- Emerging role of ETV4 in colorectal cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
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.
Funding
Abstract
Colorectal cancer (CRC) lethality is largely driven by liver metastasis and the associated tumor microenvironment (TME). This study identifies ETS variant transcription factor 4 (ETV4) as a central integrator of oncogenic signaling, metabolism, and stromal remodeling. In CRC cells, hepatocyte growth factor (HGF)/MET signaling induces ETV4 via an ERK1/2-p65 pathway. ETV4, in turn, directly activates MET and asparagine synthetase (ASNS), creating a positive feedback loop that amplifies MET signaling and elevates intracellular asparagine (Asn). Tumor-derived Asn acts as a paracrine signal that induces inflammatory cancer-associated fibroblast (iCAF) like activation in hepatic stellate cells (HSCs) and promotes iCAF polarization in primary CAFs, leading to enhanced HGF secretion that further stimulates MET
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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.