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Urinary PGE-M in Men with Prostate Cancer
Maeve Kiely1, Ginger L Milne2, Tsion Z Minas1
1Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Abstract:
Urinary PGE-M is a stable metabolite of prostaglandin E2 (PGE2). PGE2 is a product of the inflammatory COX signaling pathway and has been associated with cancer incidence and metastasis. Its synthesis can be inhibited by aspirin. We investigated the association of PGE-M with lethal prostate cancer in a case-control study of African American (AA) and European American men. We measured urinary PGE-M using mass-spectrometry. Samples were obtained from 977 cases and 1022 controls at the time of recruitment. We applied multivariable logistic and Cox regression modeling to examine associations of PGE-M with prostate cancer and participant survival. Median survival follow-up was 8.4 years, with 246 deaths among cases. Self-reported aspirin use over the past 5 years was assessed with a questionnaire. Race/ethnicity was self-reported. Urinary PGE-M levels did not differ between men with prostate cancer and population-based controls. We observed no association between PGE-M and aggressive disease nor prostate-cancer-specific survival. However, we observed a statistically significant association between higher (>median) PGE-M and all-cause mortality in AA cases who did not regularly use aspirin (HR = 2.04, 95% CI 1.23-3.37). Among cases who reported using aspirin, there was no association. Our study does not support a meaningful association between urinary PGE-M and prostate cancer. Moreover, PGE-M levels were not associated with aggressive prostate cancer. However, the observed association between elevated PGE-M and all-cause mortality in AA non-aspirin users reinforces the potential benefit of aspirin to reduce mortality among AA men with prostate cancer.
Insights
Urinary prostaglandin E2 metabolite (PGE-M) levels were not linked to prostate cancer risk or aggressive disease. However, higher PGE-M correlated with increased mortality in African American men with prostate cancer who did not use aspirin.
Area of Science:
- Oncology
- Biochemistry
- Epidemiology
Background:
- Prostaglandin E2 (PGE2), a product of the COX inflammatory pathway, is implicated in cancer development and metastasis.
- Aspirin is known to inhibit PGE2 synthesis.
- Urinary PGE-M serves as a stable metabolite for assessing PGE2 levels.
Purpose of the Study:
- To investigate the association between urinary PGE-M and lethal prostate cancer in African American and European American men.
- To examine the relationship between PGE-M levels and prostate cancer aggressiveness and survival.
Main Methods:
- A case-control study involving 977 prostate cancer cases and 1022 controls.
- Urinary PGE-M measured via mass spectrometry.
- Multivariable logistic and Cox regression models used to analyze associations with survival and disease, considering race and aspirin use.
Main Results:
- No significant difference in urinary PGE-M levels between prostate cancer cases and controls.
- PGE-M was not associated with aggressive prostate cancer or prostate cancer-specific survival.
- Higher PGE-M was linked to increased all-cause mortality in African American cases not using aspirin (HR=2.04), but not in aspirin users.
Conclusions:
- Urinary PGE-M is not a significant indicator for prostate cancer risk or aggressive disease.
- Elevated PGE-M may be associated with higher all-cause mortality in African American men with prostate cancer who do not use aspirin.
- Findings suggest a potential mortality-reducing benefit of aspirin for African American men with prostate cancer.
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