ArticleCancer prevention research (Philadelphia, Pa.)2025
Effect Modification by Levels of Sex Hormones in the Association between Adiposity and Cancer Incidence in the UK Biobank.
Article in Cancer prevention research (Philadelphia, Pa.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 2 of them syntheses 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, 2 syntheses or guidelines pooled it.
- Adiposity and cancer: systematic review and meta-analysis.Nature metabolism · 2026Pooled it
- Sex-based heterogeneity in response to first-line immunotherapy plus chemotherapy in advanced esophageal squamous-cell carcinoma: a meta-analysis.Frontiers in immunology · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The role of sex hormones in the sex difference between adiposity and cancer risk remains unclear. We examined body mass index (BMI) and visceral adipose tissue (VAT) estimated using a validated equation in relation to cancer incidence according to serum sex hormone-binding globulin (SHBG), testosterone, and estradiol among 451,500 UK Biobank participants. For cancers showing a sex-specific adiposity association, we used Cox regression to calculate multivariable HRs per increase between the 10th and 90th percentiles of adiposity according to low versus high sex hormone levels. We documented 42,949 cancers over a median follow-up of 13.1 years. BMI and VAT were more strongly associated with a higher risk of esophageal, liver, and colorectal cancers in males than in females. In males, BMI showed a stronger association with esophageal (HR for high vs. low SHBG = 2.38 vs. 1.62; Pinteraction = 0.04) and liver cancers (HR = 3.24 vs. 1.96; Pinteraction = 0.03) among those with high versus low SHBG, whereas an opposite pattern was observed for colorectal cancer (HR = 1.12 vs. 1.47; Pinteraction = 0.03). Among females, BMI was associated with a higher esophageal cancer risk in those with low (HR = 1.68) but not high SHBG (HR = 0.64; Pinteraction = 0.025); for liver cancer, results were similar but statistically nonsignificant. No interaction by estradiol or testosterone was detected. Similar results were observed for VAT. SHBG may be an important factor underlying the sex difference in adiposity-associated risk for colorectal, esophageal, and liver cancers. PREVENTION RELEVANCE: Understanding the interactions between sex hormones and adiposity can help explain sex differences in cancer risk associated with body fat. Our findings suggest that SHBG may be a promising target for future research on strategies to reduce the risk of colorectal, esophageal, and liver cancers in individuals with excess adiposity.
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Registered trials
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