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Updated: Jan 6, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Assessing the relationship between cardiometabolic diseases and the risk of developing aggressive prostate cancer: a
Aurmin J Amirmokri1, Christopher A Loffredo2, Kepher H Makambi3
1Epidemiology Program, Graduate School of Arts and Sciences, Georgetown University, Washington, DC, USA. aja171@georgetown.edu.
Background:
Prostate cancer is the most prevalent cancer among men within the U.S. and globally, with rising incidence, including advanced-staged disease. Risk factors for aggressive prostate cancer are not well defined. This systematic review and meta-analysis provide an overview of the relationship between cardiometabolic diseases (diabetes, dyslipidemia, obesity, and hypertension) and aggressive prostate cancer.
Methods:
Aggressive prostate cancer was defined as disease that has spread or is at high risk of spreading: high-risk or very high-risk localized (T3-T4, Grade Group 4-5), node-positive (N1), or metastatic (M1). Using PRISMA guidelines, a total of 4,830 publications revealed 25 cohort studies of over 974,000 men. Following the systematic review of these prospective studies of men with prostate cancer, R was utilized to run a random effects model, yielding hazard ratios with 95% confidence intervals and generating forest plots with measures of heterogeneity.
Results:
Examination of these studies revealed that a positive association exists. Diabetes was associated with a significantly increased risk of aggressive prostate cancer (HR = 1.18; 95% CI: 1.07-1.30; p = 0.0008). Obesity also showed a significant association (HR = 1.15; 95% CI: 1.06-1.24; p = 0.0006), as did hypertension, though to a lesser degree (HR = 1.07; 95% CI: 1.00-1.14; p = 0.04). Dyslipidemia was not significantly associated with aggressive prostate cancer (HR = 1.03; 95% CI: 0.98-1.03; p = 0.26).
Discussion:
Three of the four cardiometabolic disease components (diabetes, obesity and hypertension) were shown to have statistical significance and offered intriguing evidence on their potential associations with aggressive prostate cancer. Dyslipidemia's association was not statistically significant, which could be attributed to variations in methods of assessment and differing mechanistic effects. High heterogeneity and limited study availability remain key limitations.
Conclusion:
If such associations between cardiometabolic diseases and prostate cancer aggressiveness are shown to be cause and effect, such controllable and treatable conditions can allow oncologists to work alongside primary care physicians to improve patient outcomes and reduce the incidence of aggressive disease. Through the promotion of lifestyle modifications, tighter cardiometabolic control, and targeted interventions, public health efforts might improve prostate cancer outcomes.
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