Original Article

Clinical Research

Periprostatic adipose inflammation is associated with high-grade prostate cancer

  • Prostate Cancer and Prostatic Diseases volume 20, pages 418423 (2017)
  • doi:10.1038/pcan.2017.31
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Abstract

Background:

Obesity, a cause of subclinical inflammation, is associated with increased risk of high-grade prostate cancer (PC) and poor outcomes. Whether inflammation occurs in periprostatic white adipose tissue (WAT), and contributes to the negative impact of obesity on PC aggressiveness, is unknown.

Methods:

In a single-center, cross-sectional design, men with newly diagnosed PC undergoing radical prostatectomy were eligible for study participation. The primary objective was to examine the prevalence of periprostatic WAT inflammation defined by the presence of crown-like structures (CLS-P) as detected by CD68 immunohistochemistry. Secondary objectives were to explore the clinical and systemic correlates of periprostatic WAT inflammation. Tumor characteristics and host factors including BMI, adipocyte diameter, and circulating levels of lipids, adipokines, and other metabolic factors were measured. Wilcoxon rank-sum, Chi-square, or Fisher’s exact tests, and generalized linear regression were used to examine the association between WAT inflammation and tumor and host characteristics.

Results:

Periprostatic fat was collected from 169 men (median age 62 years; median BMI 28.3). Periprostatic WAT inflammation was identified in 49.7% of patients and associated with higher BMI (P=0.02), larger adipocyte size (P=0.004) and Gleason grade groups IV/V tumors (P=0.02). The relationship between WAT inflammation and high Gleason grade remained significant after adjusting for BMI (P=0.04). WAT inflammation correlated with higher circulating levels of insulin, triglycerides, and leptin/adiponectin ratio, and lower high density lipoprotein cholesterol, compared to those without WAT inflammation (P’s <0.05).

Conclusion:

Periprostatic WAT inflammation is common in this cohort of men with PC and is associated with high-grade PC.

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Acknowledgements

We thank all the patients who generously volunteered to participate in this study. This work was supported by the Prostate Cancer Foundation (Movember-Challenge Award), Patricia and William Kleh, and Memorial Sloan Kettering Cancer Center Support Grant/Core Grant (P30 CA008748). LWJ is supported by grants from the National Cancer Institute and Aktiv Against Cancer.

Author information

Affiliations

  1. Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA

    • A Gucalp
    • , N M Iyengar
    • , S Williams
    • , M D Krasne
    • , P G Morris
    • , L W Jones
    • , C A Hudis
    •  & H I Scher
  2. Department of Medicine, Weill Cornell Medical College, New York, NY, USA

    • A Gucalp
    • , N M Iyengar
    • , I Yaghnam
    • , L W Jones
    • , C A Hudis
    • , H I Scher
    •  & A J Dannenberg
  3. Department of Healthcare Policy and Research, Weill Cornell Medical College, New York, NY, USA

    • X K Zhou
    •  & H Wang
  4. Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA

    • D D Giri
  5. Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY, USA

    • D J Falcone
  6. Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA

    • B Kunzel
    • , V P Laudone
    • , P T Scardino
    •  & J A Eastham
  7. Departments of Medicine and Oncology, McGill University, Montreal, Quebec, Canada

    • M Pollak

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Competing interests

The authors declare no conflict of interest.

Corresponding author

Correspondence to A J Dannenberg.