ArticleArchives of medical science : AMS2026
Dissecting the potential impact of appendectomy on colorectal cancer through metabolites and inflammatory proteins: a Mendelian randomization study.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Introduction: Traditional longitudinal epidemiological investigations have demonstrated an association between appendectomy and the cumulative incidence of colorectal cancer (CRC). However, there is a paucity of evidence for a causal relationship between appendectomy and CRC from alternative methodologies. Material and methods: We extracted summary statistics for CRC, appendectomy, 1,400 metabolites, and 91 inflammatory proteins from the largest European ancestry genome-wide association studies (GWAS) and the FinnGen study. Using two-sample bidirectional Mendelian randomization (MR), we explored the potential causal relationship between genetic liability to appendectomy and CRC. Moreover, we employed a two-step MR approach to identify metabolites and inflammatory proteins that may mediate the effects of genetic liability to appendectomy on CRC risk and analyzed their potential mediator variables. Furthermore, we used the significant single nucleotide polymorphisms (SNPs) associated with the risk of CRC due to appendectomy, searched for the nearest genes in the FinnGen, and explored the relationship between these genes and CRC prognosis by analyzing transcriptomic data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). Results: Two-sample MR analysis revealed evidence supporting a potential causal effect of genetic liability to appendectomy on an increased risk of CRC. Two-step MR analysis identified carnitine and interleukin-13 (IL-13) as key mediators potentially involved in the positive causal relationship between genetic liability to appendectomy and CRC. Survival analysis showed that upregulation of HLX and OSR1 expression is positively correlated with poor prognosis in CRC patients. Conclusions: This MR investigation provides evidence supporting a potential causal relationship between genetic liability to appendectomy and CRC, with carnitine and IL-13 potentially acting as partial mediators of this effect.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.