Observational studyBMC cancer2025
Complex interplay between type 2 diabetes mellitus and pancreatic cancer: insights from observational and mendelian randomization analyses.
Observational study in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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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, 1 synthesis or guideline pooled it.
- Type 2 diabetes mellitus and cancer: A systematic review and meta-analysis of Mendelian randomization studies.Frontiers in endocrinology · 2026Pooled it
- Metabolic reprogramming in diabetes and cancer: the role of PI3K/AKT/mTOR and beyond.American journal of cancer research · 2026Review
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
Abstract
backgroundTo investigate the causal relationship between type 2 diabetes mellitus (T2DM), pancreatic cancer (PC) risk and identify the mediating effects of various risk factors on that relationship.
methods581 PC patients and 582 healthy controls who visited our center from January 2013 to December 2023 were included in this retrospective study. Multivariable logistic regression was performed to evaluate the association between T2DM and PC through odds ratios (ORs) and 95% confidence intervals (CIs). Mendelian randomization (MR) studies were then conducted to explore the causal relationship between T2DM and PC, and causal mediation analysis (CMA) to examine the mediating role of common risk factors.
resultsAfter adjusting for confounding factors, retrospective analysis revealed significant association between new-onset diabetes mellitus (NODM) and PC risk, with insulin treatment also linked to increased PC development. The standard inverse-variance weighted (IVW) method indicated that genetic susceptibility to T2DM was associated with an increased risk of developing PC (OR = 1.11; 95% CI = 1.034-1.193). Furthermore, MR showed T2DM, insulin treatment, FGF-4, and sulfhydryl oxidase 2 may be independently associated with the prevalence of PC. Specially, CMA demonstrated that insulin treatment, FGF4, and sulfhydryl oxidase 2 mediate the pathway from T2DM to PC, contributing 56.8%, 55.8%, and 5.9% of the total effect, respectively.
conclusionThis study supports the association between T2DM, specifically NODM, and increased PC risk, with insulin therapy, FGF4, and sulfhydryl oxidase 2 mediating this pathway. Further research is required to elucidate the mechanisms underlying these mediating effects. CLINICAL TRIAL NUMBER: not applicable.
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