Original Article

Clinical Research

The combination of histological prostate atrophy and inflammation is associated with lower risk of prostate cancer in biopsy specimens

  • Prostate Cancer and Prostatic Diseases volume 20, pages 413417 (2017)
  • doi:10.1038/pcan.2017.30
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Abstract

Background:

To evaluate whether the presence of both prostate atrophy (PA) and chronic prostate inflammation (CPI) in the same biopsy and in the same biopsy core are associated with prostate cancer (PCa) risk and grade in repeat biopsies.

Methods:

Retrospective analyses of 6132 men who were 50–75 years old undergoing 2-year repeat prostate biopsy after a negative baseline biopsy for PCa in the REduction by DUtasteride of prostate Cancer Events (REDUCE) study. PA, CPI and PCa were determined by central pathology. The association of baseline PA and CPI with 2-year repeat biopsy cancer status and grade was evaluated with χ2 test and logistic regression controlling clinicopathological features.

Results:

PA, CPI and both were detected in 583 (9.5%), 1063 (17.4%) and 3675 (59.9%) baseline biopsies, respectively. Compared with biopsies with neither PA nor CPI, the presence of PA (odds ratio (OR)=0.73, 95% confidence interval (CI)=0.57–0.93), CPI (OR=0.72, 95% CI=0.58–0.88) and both (OR=0.54, 95% CI=0.45–0.64) were associated with lower PCa risk in the 2-year repeat prostate biopsy. Results were similar in multivariable analysis. Among subjects with both PA and CPI, those with both findings in the same core had even lower PCa risk compared with PA and CPI in different cores (univariable OR=0.68, 95% CI=0.51–0.91; multivariable OR=0.73, 95% CI=0.54–0.99). Combination of PA and CPI was associated with lower risk of high-grade PCa.

Conclusions:

The presence of both PA and CPI in baseline biopsies, especially in the same core, was associated with lower PCa risk and grade. The presence and topographical distribution of PA and CPI may be used in PCa risk stratification.

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Acknowledgements

Data were provided by GSK. No funding was provided for this study.

Author information

Affiliations

  1. Department of Urology, University of Illinois at Chicago, Chicago, IL, USA

    • D M Moreira
  2. University of Southern California, Los Angeles, CA, USA

    • D M de O Freitas
  3. Nossa Senhora da Conceição Hospital, Porto Alegre, Brazil

    • D M de O Freitas
  4. Department of Urology, Queen's University, Kingston, ON, Canada

    • J C Nickel
  5. Division of Urologic Surgery, Department of Surgery, Washington University School of Medicine, St Louis, MO, USA

    • G L Andriole
  6. GlaxoSmithKline, Global R&D, King of Prussia, Pennsylvania, PA, USA

    • R Castro-Santamaria
  7. Division of Urology, Department of Surgery, Cedars Sinai Medical Center, Los Angeles, CA, USA

    • S J Freedland

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Competing interests

I certify that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/ affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received or pending) are the following: DdOF, JCN and DMM have no disclosures; GLA Jr: consulting and advisory board (GlaxoSmithKline, PLC), speaker fees (GlaxoSmithKline, PLC), research support (GlaxoSmithKline, PLC); RC-S: employee (GlaxoSmithKline, PLC); SF: research support (GlaxoSmithKline, PLC)

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Corresponding author

Correspondence to D M Moreira.

Supplementary information

Supplementary Information accompanies the paper on the Prostate Cancer and Prostatic Diseases website (http://www.nature.com/pcan)