Inflammation in benign prostate tissue and prostate cancer in the finasteride arm of the prostate cancer prevention trial

Teemu J. Murtola, Bora Gurel, Martin Umbehr, M. Scott Lucia, Ian M. Thompson, Phyllis J. Goodman, Alan R. Kristal, Howard L. Parnes, Scott M. Lippman, Siobhan Sutcliffe, Sarah B. Peskoe, John R. Barber, Charles G. Drake, William G Nelson, Angelo Michael Demarzo, Elizabeth A Platz

Research output: Contribution to journalArticle

Abstract

Background: A previous analysis of the placebo arm of the Prostate Cancer Prevention Trial (PCPT) reported 82% overall prevalence of intraprostatic inflammation and identified a link between inflammation and higher-grade prostate cancer and serum PSA. Here, we studied these associations in the PCPT finasteride arm. Methods: Prostate cancer cases (N=197) detected either on a clinically indicated biopsy or on protocol-directed end-ofstudy biopsy, and frequency-matched controls (N=248) with no cancer on an end-of-study biopsy were sampled from the finasteride arm. Inflammation in benign prostate tissue was visually assessed using digital images of hematoxylin and eosin-stained sections. Logistic regression was used for statistical analysis. Results: In the finasteride arm, 91.6% of prostate cancer cases and 92.4% of controls had at least one biopsy core with inflammation in benign areas (P <0.001 for difference compared with placebo arm). Overall, the odds of prostate cancer did not differ by prevalence [OR, 0.90;95%confidence interval (CI), 0.44-1.84] or extent (P trend=0.68) of inflammation. Inflammation was not associated with higher-grade disease (prevalence: OR, 1.07; 95% CI, 0.43-2.69). Furthermore, mean PSA concentration did not differ by the prevalence or extent of inflammation in either cases or controls. Conclusion: The prevalence of intraprostatic inflammation was higher in the finasteride than placebo arm of the PCPT, with no association with higher-grade prostate cancer. Impact: Finasteride may attenuate the association between inflammation and higher-grade prostate cancer. Moreover, the missing link between intraprostatic inflammation and PSA suggests that finasteride may reduce inflammation-associated PSA elevation. Cancer Epidemiol Biomarkers Prev; 25(3); 463-9.

Original languageEnglish (US)
Pages (from-to)463-469
Number of pages7
JournalCancer Epidemiology Biomarkers and Prevention
Volume25
Issue number3
DOIs
StatePublished - Mar 1 2016

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Finasteride
Prostate
Prostatic Neoplasms
Inflammation
Biopsy
Placebos
Confidence Intervals
Hematoxylin
Eosine Yellowish-(YS)
Tumor Biomarkers
Logistic Models

ASJC Scopus subject areas

  • Epidemiology
  • Oncology

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Inflammation in benign prostate tissue and prostate cancer in the finasteride arm of the prostate cancer prevention trial. / Murtola, Teemu J.; Gurel, Bora; Umbehr, Martin; Lucia, M. Scott; Thompson, Ian M.; Goodman, Phyllis J.; Kristal, Alan R.; Parnes, Howard L.; Lippman, Scott M.; Sutcliffe, Siobhan; Peskoe, Sarah B.; Barber, John R.; Drake, Charles G.; Nelson, William G; Demarzo, Angelo Michael; Platz, Elizabeth A.

In: Cancer Epidemiology Biomarkers and Prevention, Vol. 25, No. 3, 01.03.2016, p. 463-469.

Research output: Contribution to journalArticle

Murtola, TJ, Gurel, B, Umbehr, M, Lucia, MS, Thompson, IM, Goodman, PJ, Kristal, AR, Parnes, HL, Lippman, SM, Sutcliffe, S, Peskoe, SB, Barber, JR, Drake, CG, Nelson, WG, Demarzo, AM & Platz, EA 2016, 'Inflammation in benign prostate tissue and prostate cancer in the finasteride arm of the prostate cancer prevention trial', Cancer Epidemiology Biomarkers and Prevention, vol. 25, no. 3, pp. 463-469. https://doi.org/10.1158/1055-9965.EPI-15-0987
Murtola, Teemu J. ; Gurel, Bora ; Umbehr, Martin ; Lucia, M. Scott ; Thompson, Ian M. ; Goodman, Phyllis J. ; Kristal, Alan R. ; Parnes, Howard L. ; Lippman, Scott M. ; Sutcliffe, Siobhan ; Peskoe, Sarah B. ; Barber, John R. ; Drake, Charles G. ; Nelson, William G ; Demarzo, Angelo Michael ; Platz, Elizabeth A. / Inflammation in benign prostate tissue and prostate cancer in the finasteride arm of the prostate cancer prevention trial. In: Cancer Epidemiology Biomarkers and Prevention. 2016 ; Vol. 25, No. 3. pp. 463-469.
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abstract = "Background: A previous analysis of the placebo arm of the Prostate Cancer Prevention Trial (PCPT) reported 82{\%} overall prevalence of intraprostatic inflammation and identified a link between inflammation and higher-grade prostate cancer and serum PSA. Here, we studied these associations in the PCPT finasteride arm. Methods: Prostate cancer cases (N=197) detected either on a clinically indicated biopsy or on protocol-directed end-ofstudy biopsy, and frequency-matched controls (N=248) with no cancer on an end-of-study biopsy were sampled from the finasteride arm. Inflammation in benign prostate tissue was visually assessed using digital images of hematoxylin and eosin-stained sections. Logistic regression was used for statistical analysis. Results: In the finasteride arm, 91.6{\%} of prostate cancer cases and 92.4{\%} of controls had at least one biopsy core with inflammation in benign areas (P <0.001 for difference compared with placebo arm). Overall, the odds of prostate cancer did not differ by prevalence [OR, 0.90;95{\%}confidence interval (CI), 0.44-1.84] or extent (P trend=0.68) of inflammation. Inflammation was not associated with higher-grade disease (prevalence: OR, 1.07; 95{\%} CI, 0.43-2.69). Furthermore, mean PSA concentration did not differ by the prevalence or extent of inflammation in either cases or controls. Conclusion: The prevalence of intraprostatic inflammation was higher in the finasteride than placebo arm of the PCPT, with no association with higher-grade prostate cancer. Impact: Finasteride may attenuate the association between inflammation and higher-grade prostate cancer. Moreover, the missing link between intraprostatic inflammation and PSA suggests that finasteride may reduce inflammation-associated PSA elevation. Cancer Epidemiol Biomarkers Prev; 25(3); 463-9.",
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T1 - Inflammation in benign prostate tissue and prostate cancer in the finasteride arm of the prostate cancer prevention trial

AU - Murtola, Teemu J.

AU - Gurel, Bora

AU - Umbehr, Martin

AU - Lucia, M. Scott

AU - Thompson, Ian M.

AU - Goodman, Phyllis J.

AU - Kristal, Alan R.

AU - Parnes, Howard L.

AU - Lippman, Scott M.

AU - Sutcliffe, Siobhan

AU - Peskoe, Sarah B.

AU - Barber, John R.

AU - Drake, Charles G.

AU - Nelson, William G

AU - Demarzo, Angelo Michael

AU - Platz, Elizabeth A

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N2 - Background: A previous analysis of the placebo arm of the Prostate Cancer Prevention Trial (PCPT) reported 82% overall prevalence of intraprostatic inflammation and identified a link between inflammation and higher-grade prostate cancer and serum PSA. Here, we studied these associations in the PCPT finasteride arm. Methods: Prostate cancer cases (N=197) detected either on a clinically indicated biopsy or on protocol-directed end-ofstudy biopsy, and frequency-matched controls (N=248) with no cancer on an end-of-study biopsy were sampled from the finasteride arm. Inflammation in benign prostate tissue was visually assessed using digital images of hematoxylin and eosin-stained sections. Logistic regression was used for statistical analysis. Results: In the finasteride arm, 91.6% of prostate cancer cases and 92.4% of controls had at least one biopsy core with inflammation in benign areas (P <0.001 for difference compared with placebo arm). Overall, the odds of prostate cancer did not differ by prevalence [OR, 0.90;95%confidence interval (CI), 0.44-1.84] or extent (P trend=0.68) of inflammation. Inflammation was not associated with higher-grade disease (prevalence: OR, 1.07; 95% CI, 0.43-2.69). Furthermore, mean PSA concentration did not differ by the prevalence or extent of inflammation in either cases or controls. Conclusion: The prevalence of intraprostatic inflammation was higher in the finasteride than placebo arm of the PCPT, with no association with higher-grade prostate cancer. Impact: Finasteride may attenuate the association between inflammation and higher-grade prostate cancer. Moreover, the missing link between intraprostatic inflammation and PSA suggests that finasteride may reduce inflammation-associated PSA elevation. Cancer Epidemiol Biomarkers Prev; 25(3); 463-9.

AB - Background: A previous analysis of the placebo arm of the Prostate Cancer Prevention Trial (PCPT) reported 82% overall prevalence of intraprostatic inflammation and identified a link between inflammation and higher-grade prostate cancer and serum PSA. Here, we studied these associations in the PCPT finasteride arm. Methods: Prostate cancer cases (N=197) detected either on a clinically indicated biopsy or on protocol-directed end-ofstudy biopsy, and frequency-matched controls (N=248) with no cancer on an end-of-study biopsy were sampled from the finasteride arm. Inflammation in benign prostate tissue was visually assessed using digital images of hematoxylin and eosin-stained sections. Logistic regression was used for statistical analysis. Results: In the finasteride arm, 91.6% of prostate cancer cases and 92.4% of controls had at least one biopsy core with inflammation in benign areas (P <0.001 for difference compared with placebo arm). Overall, the odds of prostate cancer did not differ by prevalence [OR, 0.90;95%confidence interval (CI), 0.44-1.84] or extent (P trend=0.68) of inflammation. Inflammation was not associated with higher-grade disease (prevalence: OR, 1.07; 95% CI, 0.43-2.69). Furthermore, mean PSA concentration did not differ by the prevalence or extent of inflammation in either cases or controls. Conclusion: The prevalence of intraprostatic inflammation was higher in the finasteride than placebo arm of the PCPT, with no association with higher-grade prostate cancer. Impact: Finasteride may attenuate the association between inflammation and higher-grade prostate cancer. Moreover, the missing link between intraprostatic inflammation and PSA suggests that finasteride may reduce inflammation-associated PSA elevation. Cancer Epidemiol Biomarkers Prev; 25(3); 463-9.

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