DOI: 10.1097/01.cco.0000158733.61228.48

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PMID: 15818170

Issn Print: 1040-8746

Publication Date: 2005/05/01


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Questions without answers

Frank M Torti; Mebea Aklilu

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Data from the control arm of the prostate prevention trial have given us a new, useful view of the natural history and progression of prostate cancer. There were two “surprises” in this trial. First, a substantial proportion of those men had the diagnosis of prostate cancer made with a PSA under 4.0. Of men with a PSA under 0.5 ng/ml, 6.6% were diagnosed with prostate cancer, as were 10.1% of men with values between 0.6 and 1.0 ng/ml, 17% in the 1.1-2.0 ng/ml range, 23.9% between 2.1-3.0, and 26.9% between 3.1 and 4. High-grade cancers doubled from 12.5% in the lowest PSA range to 25% in the highest range [1]. Although such findings had been observed and predicted in smaller studies, the size and clarity of the results in this trial raised troubling and unsettled issues regarding prostate screening. The second surprise was the high incidence rate of prostate cancer in the population; roughly 15% of men followed for 7 years developed histologically confirmed prostate cancer. This was a substantially higher percentage of men than originally predicted.
Clearly, in the era of widespread PSA screening, prostate cancer can be diagnosed. But in a disease that has a death rate in men older than 65 of only 226 per 100,000, many patients will be treated who will not develop life-threatening disease. Stamey et al. [2] reported on 1317 consecutive prostatectomies performed after the introduction of screening PSA from 1983 to 2003. They found that while PSA screening had some correlation with prostate cancer volume and morphologic variables in the first 10 years of the study, in the past 5 years PSA correlated with benign prostatic hypertrophy only [2].
At present, no conclusive proof demonstrates a decline in mortality as a result of prostate cancer screening with PSA. The ongoing Prostate, Lung, Colorectal and Ovarian Cancer Screening trial sponsored by the National Cancer Institute as well as the European Randomized Study of Screening for Prostate Cancer should help answer that question. It is clear that a biomarker that can distinguish between an aggressive tumor from one that will not have any clinical impact must be identified and developed.
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