Evidence map›Paper›PMID 40172743›Full record

ArticleDiscover oncology2025

A mendelian randomization study on the association between type 2 diabetes and the risk of bladder cancer.

Yuan He, Yu Chen, Chang Gao

Abstract read
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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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3 · Its place in the literature

Who cites it

3 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

3 authors.

Yuan HeDepartment of Endocrinology, Second Hospital of Tianjin Medical University, No.23 of Pingjiang Road, Hexi District, Tianjin, 300211, China. heyuanhyf@126.com.
Yu ChenDepartment of Endocrinology, Second Hospital of Tianjin Medical University, No.23 of Pingjiang Road, Hexi District, Tianjin, 300211, China.
Chang GaoDepartment of Endocrinology, Second Hospital of Tianjin Medical University, No.23 of Pingjiang Road, Hexi District, Tianjin, 300211, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeWe used Mendelian randomization (MR) analyses to examine the potential causal effects of type 2 diabetes and glycemic traits on bladder cancer risk.

methodsTwo-sample MR analyses were conducted using summary data from genome-wide association studies (GWAS). Exposures included type 2 diabetes, fasting glucose, glycosylated hemoglobin (HbA1c), fasting insulin, and proinsulin levels, with bladder cancer as the outcome. Four methods-inverse variance weighted, MR-Egger, weighted median, and weighted mode-were used to assess the causal effects. Sensitivity analyses were conducted to ensure that the results were robust.

resultsIn the inverse variance weighted model, a weak positive effect was detected between genetically predicted HbA1c and bladder cancer (OR = 1.003, 95% CI = 1.0001 to 1.0052, P = 0.043). Other MR methods produced results with the same trend, although not all were statistically significant. However, there was no evidence to support the effect of type 2 diabetes, fasting insulin, or proinsulin levels on bladder cancer. No significant heterogeneity or pleiotropy was detected.

conclusionMendelian randomization analysis indicated a mild promoting effect of increased HbA1c levels on bladder cancer risk. Further studies with larger sample sizes are needed to confirm this hypothesis.

Indexed as

Bladder cancerCausal effectGlycemic traitsMendelian randomizationType 2 diabetes

Identifiers

PMID40172743
PMCPMC11965069

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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 OpenQuestion graph.