Proteomics of multimorbidity progression across cardiometabolic diseases and cancer in a multinational cohort
Authors' conclusion
This study identifies candidate proteins that may indicate molecular pathways to multimorbidity of cardiometabolic diseases and cancer. Future studies should evaluate the causal roles of these proteins for targeted interventions and risk stratification.
Study context
- Population
- EPIC participants; multimorbidity of CVD, T2D and/or cancer modelled as sequential disease transitionsUK Biobank replication N = 44,567
- Participants
- 13,270 participants
- Outcome
- Protein signatures (SomaScan 7k; 7,289 aptamers) of multimorbidity progression: disease-free → first disease → second disease (cancer, CVD, T2D)
Methodological detailsproteomics, multinational, weighted multivariable Cox regression, replication in UK Biobank (Olink)
- Proteomics
- Multinational
- Weighted multivariable Cox regression
- Replication in UK Biobank (Olink)
Main finding
As reported in the abstract
Aptamers associated with multimorbidity
- Aptamers associated with >1 disease (FDR-corrected P < 0.05)
- 422
- Aptamers shared between CVD and T2D
- 265
- Aptamers associated with multimorbidity progression
- 38
- Aptamers with consistent positive associations across sequential transitions
- 27
- SEMA6A, disease-free to cancer: HR
- 1.14 (95% CI 1.05, 1.23)
- SEMA6A, cancer to T2D: HR
- 2.61 (95% CI 1.76, 3.80)
- Aptamers with consistent inverse associations
- 4
- NLGN1, disease-free to T2D: HR
- 0.72 (95% CI 0.61, 0.84)
- NLGN1, T2D to cancer: HR
- 0.57 (95% CI 0.43, 0.75)
Observational data: associations, not effects.
Further findings
Replication in UK Biobank (Olink)
- Identified proteins also measured in UK Biobank, with broadly consistent associations
- 19
Original publication
Proteomics of multimorbidity progression across cardiometabolic diseases and cancer in a multinational cohort. Cardiovasc Diabetol. Published 20 June 2026. doi:10.
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