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Accelerated biological aging with bladder and kidney cancer compared to prostate cancer or non-cancer controls: A UK Biobank study
Heather McClure, BS
1, Alison Kim, MPH
1, Shanshu Zhao, BS
2, George A. Kuchel, MD
3, Chia-Ling Kuo, PhD
3,
Benjamin T. Ristau, MD, MHA4.
1University of Connecticut School of Medicine, Farmington, CT, USA,
2University of Connecticut Graduate School, Farmington, CT, USA,
3UConn Health Center on Aging, Farmington, CT, USA,
4UConn Health, Farmington, CT, USA.
BACKGROUND: Age is an independent risk factor for urologic cancers. While clinicians implicitly account for chronologic age when making treatment decisions, objective assessment of biologic age is not routinely performed. PhenoAge is a validated composite measure that uses 9 blood-based biomarkers to predict biologic age. We compared the mean and variance of phenoage between cancer-free individuals and those with newly diagnosed urologic cancers.
METHODS: UK Biobank recruited over 500,000 participants age 40-70 from 2006-2010. Baseline blood samples were collected at study entry. We grouped participants based on development of urologic cancer within 5 years of study enrollment: no cancer, prostate cancer (PCa), bladder/kidney cancer (BKCa). PhenoAge, adjusted for chronologic age and other covariates, was compared between groups using a linear regression model. Heterogeneity was assessed using gamma regression model with a log link.
RESULTS: In males, PhenoAge was higher in participants with incident BKCa compared to no cancer (0.59, 95% CI 0.24-0.93 p<0.01). It was also higher with incident BKCa compared to incident PCa (0.57, 95% CI 0.19-0.96, p=0.01). There was no difference in PhenoAge between PCa and no cancer (p=1). In females, PhenoAge was greater - by 1.4 years - in participants with incident BKCa compared to no cancer (1.4, 95% CI 0.83-1.9, p<0.01). Greater PhenoAge heterogeneity was observed in BKCa compared to no cancer in both the male (p=0.01) and female (p<0.01) cohorts.
CONCLUSIONS: Using PhenoAge, we demonstrate evidence of accelerated aging in both men and women who developed BKCa compared to noncancer controls. Men with PCa did not show accelerated aging, which may be related to a lesser impact of biological aging on development of these indolent cancers. Greater PhenoAge heterogeneity in patients with BKCa may represent an opportunity to improve individual clinical outcomes by incorporating biologic aging measures into treatment decision-making.
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