ArticleMedicine2026
Causal relationship between oral microbiome, circulating inflammatory proteins and lung cancer: A Mendelian randomization study.
Article in Medicine, 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
9 authors.
Funding
Abstract
Recent research showed that oral microbiomes (OMs), as the main source of lung microbiomes, were associated with lung cancer (LC), but the causal relationship and mechanisms remain unclear. This study aimed to explore the immune mechanisms of LC through the "OM - inflammatory proteins - LC" axis. Instrumental variables covering 43 oral microbial taxa, 91 circulating inflammatory proteins, and LC subtypes were obtained from large-scale genome-wide association study summary data of European origin. We employed Mendelian randomization (MR) analysis to validate causal links between the OM and LC and to assess the mediation effects of inflammatory proteins. The primary statistical method was the inverse variance weighted method, supplemented by leave-one-out analysis, MR-Egger regression, and Cochran's Q test to assess heterogeneity and pleiotropy. Finally, we calculated the effect size of inflammatory proteins as mediators. The results suggested that 9 oral microbial taxa and 20 inflammatory proteins were significantly associated with LC and its subtypes. Key findings included: Genus Rothia increased the risk of squamous cell carcinoma. At the species level, Haemophilus parainfluenzae protected against lung adenocarcinoma, whereas Megasphaera micronuciformis prevented small cell LC. Among the inflammatory proteins, the protein S100-A12 elevated adenocarcinoma risk, and STAM binding protein increased the risk of squamous cell carcinoma. Protective proteins included artemin (squamous cell carcinoma), cystatin D (adenocarcinoma), and interleukin 18 (both subtypes mentioned above). M. micronuciformis and overall LC had a causal relationship in which cystatin D played a mediating role. This study reveals a potential causal link between the OM, circulating inflammatory proteins, and LC. The protective effect of M. micronuciformis was mediated by cystatin D, highlighting a novel immune pathway. These findings provide biomarkers for early detection of LC and therapeutic targets for LC intervention.
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.