Editorial

Nature Clinical Practice Oncology (2006) 3, 581
doi:10.1038/ncponc0653  

The evolution of the PCPT from clinical to molecular analyses

Ashraful Hoque

This article has no abstract so we have provided the first paragraph of the full text.

In the Prostate Cancer Prevention Trial (PCPT), which randomized 18,882 men with normal digital rectal examination (DRE) results and prostate-specific antigen (PSA) levels, finasteride significantly reduced prostate cancer risk by 24.8% but also increased high-grade disease (Gleason score greater than or equal to7) compared with placebo (Thompson IM et al. [2003] N Engl J Med 349: 215–224). The prevalence of prostate cancer, including high-grade tumors, was 15.2% among men with 'normal' (less than or equal to4 ng/ml) PSA levels (Thompson IM et al. [2004] N Engl J Med 350: 2239–2246); in addition, finasteride increased the sensitivity of PSA for detecting prostate cancer when compared with placebo (Thompson IM et al. [2006] J Natl Cancer Inst 98: 1128–1133). Whether the increased high-grade disease associated with finasteride was an artifact is under intensive pathological analysis and is one of several questions being addressed by a long-term follow-up study of men who developed prostate cancer during the PCPT.

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