Literature DB >> 34264335

Urinary Thromboxane B2 and Lethal Prostate Cancer in African American Men.

Maeve Kiely1, Ginger L Milne2, Tsion Z Minas1, Tiffany H Dorsey1, Wei Tang1, Cheryl J Smith1, Francine Baker1, Christopher A Loffredo3, Clayton Yates4, Michael B Cook5, Stefan Ambs1.   

Abstract

BACKGROUND: Thromboxane A2 (TXA2) is a platelet- and cyclooxygenase-derived eicosanoid that has been linked to metastasis. We investigated the role of TXA2 in the development of lethal prostate cancer in African American (AA) and European American (EA) men.
METHODS: We measured urinary 11-dehydrothromboxane B2 (TXB2), a stable metabolite of TXA2, with mass spectrometry. Samples were obtained from 977 cases and 1022 controls at time of recruitment. We applied multivariable logistic and Cox regression modeling to examine associations of TXB2 with prostate cancer and patient survival. The median survival follow-up was 8.4 years, with 246 deaths among cases. Aspirin use was assessed with a questionnaire. Race was self-reported.
RESULTS: Urinary TXB2 was inversely associated with aspirin use. High (>median) TXB2 was associated with prostate cancer in AA (adjusted odds ratio [OR] = 1.50, 95% confidence interval [CI] = 1.13 to 2.00) but not EA men (OR = 1.07, 95% CI = 0.82 to 1.40), suggesting upregulated TXA2 synthesis in AA men with prostate cancer. High TXB2 was positively associated with metastatic prostate cancer (OR = 2.60, 95% CI = 1.08 to 6.28) compared with low (≤median) TXB2. Furthermore, high TXB2 was also associated with all-cause (adjusted hazard ratio = 1.59, 95% CI = 1.06 to 2.40) and prostate cancer-specific mortality (hazard ratio = 4.74, 95% CI = 1.62 to 13.88) in AA men only.
CONCLUSIONS: We report a distinct association of TXB2 with prostate cancer outcomes in AA men. In this high-risk group of men, upregulation of TXA2 synthesis may promote metastasis and lethal disease. Our observation identifies a potential benefit of aspirin in preventing lethal prostate cancer through inhibition of TXA2 synthesis. Published by Oxford University Press 2021. This work is written by US Government employees and is in the public domain in the US.

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Year:  2022        PMID: 34264335      PMCID: PMC8755482          DOI: 10.1093/jnci/djab129

Source DB:  PubMed          Journal:  J Natl Cancer Inst        ISSN: 0027-8874            Impact factor:   13.506


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