Evidence map›Paper›PMID 39835552›Full record

ArticleCurrent medicinal chemistry2025

Mendelian Randomization and Transcriptome Data Analysis Reveal Bidirectional Causal Relationships and Mechanisms between Type 2 Diabetes and Gastric Cancer.

Junyang Ma, Yuan Gao, Shufu Hou, Shichang Cui, Jiankang Zhu

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Article in Current medicinal chemistry, 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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

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.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Junyang MaLaboratory of Metabolism and Gastrointestinal Tumor, Shandong Provincial QianFoShan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Yuan GaoNursing School of Nanchang University, Nanchang University, Nanchang, China.
Shufu HouLaboratory of Metabolism and Gastrointestinal Tumor, Shandong Provincial QianFoShan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Shichang CuiLaboratory of Metabolism and Gastrointestinal Tumor, Shandong Provincial QianFoShan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.
Jiankang ZhuLaboratory of Metabolism and Gastrointestinal Tumor, Shandong Provincial QianFoShan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan, China.

Funding

Shandong First Medical University Research Grant Fund 342601
6 · The paper itself

Abstract

introductionGastric cancer (GC) is the fifth most common cancer globally, and the relationship between type 2 diabetes mellitus (T2DM) and cancer risk remains controversial.

methodsWe performed Mendelian randomization (MR) analysis using publicly available GWAS data to assess the causal relationship between T2DM and GC, validated by heterogeneity and pleiotropy analyses. Transcriptomic data from TCGA and GEO were analyzed to identify common differentially expressed genes (DEGs). Weighted gene coexpression network analysis (WGCNA) was used to construct a prognostic risk model. Drug sensitivity and immune infiltration were evaluated using GDSC and ImmuCellAI, respectively. Additionally, gene mutation analysis was conducted using TCGA data.

resultsThe Mendelian randomization analysis revealed a causal relationship between T2DM and GC at the genetic level. Specifically, the causal effect of T2DM on GC was estimated with an odds ratio (OR) of 1.32 (95% CI: 1.12-1.56), while the reverse causal effect of GC on T2DM was estimated at an OR of 0.78 (95% CI: 0.67-0.91). Sensitivity analyses, including Cochran's Q test and the leave-one-out test, confirmed the robustness of these findings. We constructed a prognostic risk score consisting of three T2DM- related genes (CST2, PSAPL1, and C4orf48) based on transcriptome data analysis. Patients with high-risk scores exhibited significantly worse overall survival (OS) (p < 0.05). Cox regression analysis further confirmed the independent predictive value of the risk score for GC prognosis. Our predictive model demonstrated good performance, with an AUC of 0.786 in the training set and 0.757 in the validation set. Gene enrichment analysis indicated that the genes shared between T2DM and GC were associated with inflammatory response, immune response, and metabolic pathways. Tumor immune microenvironment analysis suggested that immune evasion mechanisms may play a key role in developing GC in patients with coexisting T2DM.

conclusionT2DM is associated with reduced GC risk. The risk score and model may help guide GC prognosis and management.

Indexed as

Diabetes Mellitus, Type 2Mendelian Randomization AnalysisStomach NeoplasmsTranscriptomeGene Expression ProfilingGenome-Wide Association StudyHumansPrognosisCST2Gastric cancermendelian randomizationPSAPL1.transcriptomic dataType 2 diabetes

Identifiers

PMID39835552

What Socratic holds

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Registered trials

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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 Socratic graph.