ArticleThe FEBS journal2026
High levels of serum cholesterol increase the risk of developing vessel co-opting tumors in colorectal cancer liver metastases.
Article in The FEBS journal, 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.
- YAP1‑mediated cytoplasmic‑nuclear translocation of SREBP2 promotes colorectal cancer via regulation of cholesterol metabolism.International journal of oncology · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholesterol availability has been implicated in cancer progression. Here, we demonstrate the connection between blood cholesterol concentration, the development of distinct histopathological growth patterns (HGPs) in colorectal cancer liver metastases (CRCLM), and new avenues of treatment for patients. Our study reveals that serum cholesterol levels correlate with the different HGPs, and patients on statins had desmoplastic HGPs and improved overall survival. We also demonstrate, in an in vivo mouse model, that inhibition of key modulators of cholesterol metabolism, using antiproprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, attenuated the development of CRCLM tumors, as well as the formation of vessel co-opting lesions. Our findings underscore the importance of cholesterol in CRCLM and the potential clinical application of evolocumab to mitigate the growth of these histological types of tumors in CRCLM.
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.