Inflammation has ‘etiologic link’ with prostate cancer

By Joanna Lyford, Senior medwireNews Reporter

Chronic inflammation of prostate tissue is strongly associated with subsequent development of prostate cancer, show results of a US observational study.

While unable to demonstrate causality, the findings support an etiological link between inflammation and prostate carcinogenesis and potentially open a new avenue for preventive strategies, the authors say.

Elizabeth Platz (Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland) and colleagues undertook a case–control study among 400 participants in the placebo arm of the Prostate Cancer Prevention Trial.

In the trial, men aged 55 years older with a normal digital rectal examination (DRE) and a serum prostate-specific antigen (PSA) level of 3 ng/mL or below were randomly assigned to receive study drug or placebo for 7 years. Men with raised PSA or abnormal DRE during the trial underwent prostate biopsy, and cancer-free men were biopsied at the end of the trial.

Platz and team obtained biopsy specimens from 191 men in the placebo arm who developed prostate cancer during the trial (cases) and 209 matched men in the placebo arm who remained free of cancer (controls). They assessed benign areas of each biopsy core for inflammation, grading the extent and severity of acute and chronic inflammation.

Their analysis, reported in Cancer Epidemiology, Biomarkers, & Prevention, showed that 86.2% of cases and 78.2% of controls had at least one biopsy core with inflammation, a statistically significant difference. The morphology of the inflammatory cells generally reflected chronic inflammation, say the authors.

After adjusting for age, family history and race, men with at least one biopsy core with inflammation were 1.78 times more likely to develop prostate cancer than were those with no biopsy cores showing inflammation. The odds ratio was unchanged after further adjustment for multiple risk factors.

There was also a dose–response, such that the likelihood of prostate cancer increased with the extent of biopsy cores with inflammation, from 1.61 for those with some cores to 2.19 for those with all cores, compared with zero cores.

The association between inflammation and subsequent prostate cancer held true among men with low baseline PSA levels (2 ng/mL or below) and was stronger for the development of high-grade than low-grade disease, the authors remark.

Noting that this is the first study to test directly the hypothesis that chronic inflammation is associated with prostate cancer, the team concludes: “Identifying those men at highest risk of developing aggressive disease is the first step in being able to prevent lethal prostate cancer.”

They add: “Rather than targeting interventions to all healthy men, which may result in unintended harms, if causal, the findings from our work may allow preventive interventions to be targeted to those men who would benefit the most.”

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