MedicalResearch.com: What are the main findings of the study?
Dr. De Marzo: Working as a team with Dr. Elizabeth Platz and a group of other investigators we found that men with chronic inflammation in their benign areas of their prostate biopsies had a higher chance of prostate cancer, and especially higher grade cancers, which are associated with disease aggressiveness. A key unique aspect of the study is that the samples were taken from man who were enrolled in the Prostate Cancer Prevention Trial (PCPT), a trial in which all men entering the study had a relatively low PSA, and, all men at the end of study who did not already have a diagnosis of prostate cancer were offered a prostate biopsy regardless of their PSA. This study design, unlike a standard association study, allowed us to minimize the potential bias whereby inflammation is associated itself with elevations in PSA. In this standard design approach, when cancer is detected it could artifactually appear that inflammation is associated with cancer because the inflammation was in part driving the PSA elevation, which prompted the biopsy in which cancer was detected.
MedicalResearch.com: Were any of the findings unexpected?
Dr. De Marzo: We were somewhat surprised at the high prevalence of inflammation even in men with very low serum PSA.
MedicalResearch.com: What should clinicians and patients take away from your report?
Dr. De Marzo: At this point the study does not have an immediate clinical impact. I would say that it would not be appropriate for clinicians to use the present of inflammation per se in a benign biopsy to influence their decision whether to perform a repeat biopsy on their patients. That decision should be based on other clinical features and overall suspicion level by the clinician.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Dr. De Marzo: We need additional studies, with a similar study design in which patients are not selected based on elevated PSA, in which men are biopsied longitudinally over time to see if the presence of inflammation on an initial biopsy could be predictive of cancer on subsequent biopsy. We also need additional studies characterizing the nature of the inflammatory cells that might be associated with cancer and to develop experimental model systems to determine whether and how inflammation affects prostate cancer development and progression.
Bora Gurel, M. Scott Lucia, Ian M. Thompson, Jr, Phyllis J. Goodman, Catherine M. Tangen, Alan R. Kristal, Howard L. Parnes, Ashraful Hoque, Scott M. Lippman, Siobhan Sutcliffe, Sarah B. Peskoe, Charles G. Drake, William G. Nelson, Angelo M. De Marzo, and Elizabeth A. Platz