ArticleInternational journal of molecular sciences2024
Strengthening the Evidence for a Causal Link between Type 2 Diabetes Mellitus and Pancreatic Cancer: Insights from Two-Sample and Multivariable Mendelian Randomization.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 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
- Diabetes and cancer: glucose control impact on survival and tumor outcomes.Reviews in endocrine & metabolic disorders · 2026Review
- Associations Between Obesity, Diabetes Mellitus, and Pancreatic Cancer in the Japanese Population: A Mendelian Randomization Study.Cancer science · 2026Article
- Prospective associations of diabetes with 15 cancers in 2.2 million UK and Chinese adults.Journal of the National Cancer Institute · 2025Article
- Genetically proxied risk and protective factors for pancreatic cancer: a systematic review and meta-analysis of Mendelian randomization studies.Journal of gastrointestinal oncology · 2025Article
- The application of mendelian randomization in cancer research: a bibliometric analysis.Discover oncology · 2025Article
- Complex interplay between type 2 diabetes mellitus and pancreatic cancer: insights from observational and mendelian randomization analyses.BMC cancer · 2025Observational
- Causal Relationship between Mitochondrial Biological Function and Periodontitis: Evidence from a Mendelian Randomization Study.International journal of molecular sciences · 2024Article
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3 authors.
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Abstract
This two-sample Mendelian randomization (MR) study was conducted to investigate the causal associations between type 2 diabetes mellitus (T2DM) and the risk of pancreatic cancer (PaCa), as this causal relationship remains inconclusive in existing MR studies. The selection of instrumental variables for T2DM was based on two genome-wide association study (GWAS) meta-analyses from European cohorts. Summary-level data for PaCa were extracted from the FinnGen and UK Biobank databases. Inverse variance weighted (IVW) and four other robust methods were employed in our MR analysis. Various sensitivity analyses and multivariable MR approaches were also performed to enhance the robustness of our findings. In the IVW and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO) analyses, the odds ratios (ORs) for each 1-unit increase in genetically predicted log odds of T2DM were approximately 1.13 for PaCa. The sensitivity tests and multivariable MR supported the causal link between T2DM and PaCa without pleiotropic effects. Therefore, our analyses suggest a causal relationship between T2DM and PaCa, shedding light on the potential pathophysiological mechanisms of T2DM's impact on PaCa. This finding underscores the importance of T2DM prevention as a strategy to reduce the risk of PaCa.
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