ArticleDiscover oncology2026
Bidirectional Mendelian randomization identifies differential causal associations between inflammatory cytokines and lung cancer subtypes.
Article in Discover oncology, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung cancer is the leading cause of cancer-related deaths globally, with non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) being its two primary subtypes. While inflammation plays a crucial role in cancer development, its specific functions in different lung cancer subtypes remain unclear.
methodsThis study employed a bidirectional two-sample Mendelian randomization (MR) approach, utilizing Genome-Wide Association Studies (GWAS) data for NSCLC (5,315 cases) and SCLC (717 cases) from the FinnGen biobank, along with 314,193 controls and GWAS data for 91 circulating inflammatory factors. We investigated the causal relationships between inflammatory factors and lung cancer risk. Instrumental variables were selected based on p-value < 1 × 10− 5 and F-statistic > 10, with linkage disequilibrium (LD) clumping (R2 <0.001, physical distance threshold 10,000 kb) applied. The primary analysis used the inverse variance weighted (IVW) method, supplemented by MR-Egger, weighted median, simple mode, and weighted mode methods for sensitivity analyses. Heterogeneity was assessed using Cochran’s Q test, horizontal pleiotropy was evaluated using the intercept term from MR-Egger regression, and bias was assessed using the MR-PRESSO global test. Additionally, we conducted sensitivity analyses to evaluate the impact of individual Single Nucleotide Polymorphisms (SNPs) on the overall causal effect estimates.
resultsFor NSCLC, Eotaxin (OR = 1.1150, 95%CI 1.0031–1.2394, P = 0.0436) and MCP-1 (OR = 1.0982, 95%CI 1.0078–1.1967, P = 0.0326) levels were positively associated with risk, while IL-12β (OR = 0.9214, 95%CI 0.8571–0.9906, P = 0.0267) and TRAIL (OR = 0.9188, 95%CI 0.8479–0.9956, P = 0.0388) levels were negatively associated with risk. For SCLC, IL-13 (OR = 1.4195, 95%CI 1.0736–1.8768, P = 0.0139), IL-17 A (OR = 1.4288, 95%CI 1.0058–2.0297, P = 0.0463), and MCP-1 (OR = 1.2898, 95%CI 1.0253–1.6224, P = 0.0297) levels were positively associated with risk, while CXCL1 (OR = 0.7448, 95%CI 0.5594–0.9915, P = 0.0435), DNER (OR = 0.7210, 95%CI 0.5265–0.9875, P = 0.0415), IL-15Rα (OR = 0.8035, 95%CI 0.6582–0.9809, P = 0.0316), and IL-18R1 (OR = 0.8090, 95%CI 0.6710–0.9753, P = 0.0262) levels were negatively associated with risk. Heterogeneity and pleiotropy tests showed no significant variables (P > 0.05). Reverse analyses did not reveal significant effects of lung cancer on these inflammatory factor levels (all p-values > 0.05).
conclusionThis study elucidated potential causal relationships between specific inflammatory factors and the risk of NSCLC and SCLC, highlighting the complex roles of different inflammatory factors in the pathogenesis of these two lung cancer subtypes. These findings provide novel insights for molecular subtyping and personalized treatment strategies in lung cancer.
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.