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Oncology outcomes

Can blood chemistry years earlier predict prostate cancer death?

Huang J, Zhao B, Zhao B, et al. · BMC medicine · 2022

Open access · cc by · source: Europe PMC

Among Finnish men who later got prostate cancer, dozens of blood metabolites measured years before diagnosis - led by choline and glutamate - were linked to a higher chance of dying from the cancer.

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Study at a glance

Design
Cohort — Case-only prospective survival analysis: 961 serum metabolites measured in fasting blood drawn at ATBC trial baseline (1985-1988) were related by Cox regression to prostate cancer death among men later diagnosed with prostate cancer, with Bonferroni correction and a 70/30 discovery-replication split.
N
N=1812 · 1812 incident prostate cancer cases from the 29,133-man ATBC cohort, of whom 472 died of prostate cancer during follow-up to the end of 2016.
Population
Finnish male smokers aged 50-69 at enrolment in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study who later developed prostate cancer.
Outcome
Prostate cancer-specific mortality after diagnosis.

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Key findings

Of the 961 metabolites, 49 were linked to prostate cancer death after Bonferroni correction. The strongest were choline (hazard ratio 2.07, top versus bottom quarter) and glutamate (hazard ratio 2.31), plus gamma-glutamyl amino acids, dipeptides and endocannabinoids; some glutathione-related metabolites were protective. Adding five selected metabolites to clinical factors improved discrimination from an AUC of 0.82 to 0.86. In the replication set, each standard-deviation rise in the risk score raised the hazard of prostate cancer death by 48%.

Methodology

The researchers used frozen fasting blood samples collected in 1985-1988 from Finnish male smokers in a large vitamin-supplement trial. For the 1812 men later diagnosed with prostate cancer, they measured 961 small molecules (metabolites) and used Cox survival models, adjusted for age, stage and Gleason score, to see which predicted death from prostate cancer. They applied a strict Bonferroni threshold for multiple testing, analysed metabolic pathways, and built a metabolite risk score in a 70% discovery set that they tested in the remaining 30%.

Limitations

The men were all Finnish smokers aged 50-69, so results may not apply to non-smokers, younger men or other ethnic groups. Replication was only internal (a random split of the same cohort), with no external validation, and tumour molecular subtypes were unavailable. As an observational study, residual confounding cannot be excluded, and associations do not show that changing these metabolites would alter survival. Metabolites were measured once, often more than a decade before diagnosis.

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