More on the topic of prostate cancer risk


Two studies published recently add some additional information to our understanding of prostate cancer risk assessment in specific groups of patients.

The first of these studies, by Xu et al., may be helpful in identifying men at considerably elevated risk and who may be particularly appropriate candidates for chemoprevention with drugs like finasteride and dutasteride.

This group of researchers showed that men with a high number of risk alleles or single-nucleotide polymorphisms (SNPs) and a positive family history of prostate cancer are at a high risk for diagnosis of prostate cancer. For example, 55-year-old men with a family history of prostate cancer and 14 or more risk alleles in Sweden and America have a 52 percent and a 41 percent risk of being diagnosed with prostate cancer in the next 20 years. By comparison, without any knowledge of their genotype and their family history, these men had an average population absolute risk of only about 13 percent.

Of course what Xu et al. can not tell us from this study is whether the prostate cancer they are at risk for is histologically evident but potentially indolent or histologically evident and potentially clinically significant!

In the second study, based on data from the UK, Pashayan et al. have explored whether stage shifting among PSA-detected prostate cancers (the effect in which more cancers are detected at an earlier stage) is affected by Gleason score.

They report that the occurrence of advanced stage disease among the PSA-detected cancers was significantly less common than among the clinically detected cancers. The PSA-detected tumors had a substantial shift to earlier-stage disease where the Gleason score was < 7 but there was no such shift if the Gleason score was 7 or more. There was also evidence of astatistically significant association between between mode of prostate cancer risk detection and Gleason score..

As the authors are careful to point out, the observed stage shift could be partially explained by length bias or by simple “overdiagnosis” of histologically evident but clinically insignificant prostate cancer.

We would be wise not to read too much into either of these studies because of our inability to tell the difference between patients with clincially significant and clinically insignificant prostate cancer at this time, but all this information does show that we are gradually accumulating the data that will help us to manage prostate cancer risk if we could only learn how to make that fundamental distinction between risk for clinically significant disease and risk for histologically evident but clinically insignificant prostate cancer.

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