ArticleMedicine2025
Cytokines and oral cancer risk: Genetic evidence from a bidirectional Mendelian randomization study.
Article in Medicine, 2025. 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to elucidate the causal relationship between cytokines and oral cancer using Mendelian randomization (MR) analysis. Utilizing genetic data from genome-wide association studies (GWAS) and publicly available datasets, we conducted a bidirectional 2-sample MR analysis. The study design employed single nucleotide polymorphisms as genetic instruments to investigate the link between cytokines and oral cancer. The analysis was based on data from 2 cohorts with total 132 cytokines: 41 cytokines from comprehensive GWAS meta-analysis data, 91 cytokines from GWAS summary statistics for circulating inflammatory cytokines. Oral cancer genetic association data was sourced from the FinGen R10 datasets. To discern the causal relationship between cytokines and oral cancer, 5 MR methodologies, including inverse variance weighted and MR-Egger regression, weighted median, weighted mode, and simple mode were applied. The MR analysis revealed nominal associations between certain cytokines and the risk of oral cancer. Specifically, increased levels of C-X-C motif chemokine ligand 9 (odd ratios [OR] = 0.760, 0.600-0.962, 95% confidence interval [CI] 0.600-0.962, P = .023), monocyte chemoattractant protein 1 (OR = 0.78, 95% CI 0.32-0.99, P = .046), and TNF related activation induced cytokine (OR = 0.792, 95% CI 0.630-0.994, P = .044) were associated with a reduced risk of oral cancer, while higher levels of monocyte chemoattractant protein 2 (OR = 1.164, 95% CI 1.001-1.353, P = .048) and CC motif chemokine 25 (OR = 1.434, 95% CI 1.106-1.858, P = .006) were linked to an increased risk. The reverse analysis suggested a possible effect of oral cancer on the level of circulating cytokines, particularly Fractalkine (OR = 0.942, 95% CI 0.897-0.990, P = .019). No evidence of heterogeneity or significant pleiotropy was detected, validating the instrumental variables used. The findings support a causal relationship between specific cytokines and the risk of oral cancer, highlighting the complex interplay between inflammatory mediators and cancer development. These results underscore the importance of individualized immune profiling in treating oral cancer patients and pave the way for future research into targeted therapies based on cytokine profiles.
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.