ArticleBritish journal of cancer2026
Anthropometric traits, metabolic biomarkers, and pancreatic cancer risk: a causal mediation analysis in UK Biobank.
Article in British journal of cancer, 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
13 authors.
Funding
Abstract
backgroundObesity is a risk factor for pancreatic cancer, but mechanisms remain unclear. We investigated how anthropometric traits, individually and combined, relate to pancreatic cancer risk and whether associations are mediated by metabolic biomarkers.
methodsWe analysed 462,300 adults (40-69 years) in the UK Biobank. Principal component analysis derived three body shape phenotypes combining body mass index (BMI), height, weight, waist and hip circumference, and waist-to-hip ratio (WHR). Mediation was assessed using four-way decomposition.
resultsOver a median follow-up of 10.9 years, 1115 pancreatic cancer cases occurred. Each one-standard-deviation (SD) increase in BMI or WHR was associated with a higher incidence of pancreatic cancer, with hazard ratios (HRs) of 1.20 (confidence interval, CI: 1.12-1.28) and 1.24 (CI: 1.14-1.36), respectively. Body shape characterizing overall obesity showed a similar association (HR = 1.20; CI: 1.12-1.28 per 1-SD), with glucose and HbA1c accounting for mediated proportions (mediated interaction + pure indirect effect) of 12.2% (CI: 3.4-21.0%) and 15.0% (CI: 5.7-24.2%), respectively. For BMI, glucose accounted for 15.9% (CI: 2.8-28.9%) and HbA1c for 20.0% (CI: 6.3-33.7%) of the association.
conclusionsGlucose and HbA1c mediate a large proportion of the obesity-pancreatic cancer association, highlighting the important role of glycemic control in obesity-related pancreatic carcinogenesis and targeted interventions in at-risk populations.
Indexed as
Identifiers
What Socratic 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 Socratic graph.