Abstract A96: The influence of infectious mononucleosis on prostate-specific antigen concentration as a marker of prostate involvement during infection

• Published in: Cancer prevention research (Philadelphia, Pa.) Pa.), 2011-10, Vol.4 (10_Supplement), p.A96-A96
• Main Authors: Sutcliffe, Siobhan, Sokoll, Lori J., Walsh, Patrick C., Zenilman, Jonathan M., Cersovsky, Steven B., Nevin, Remington L., Pakpahan, Ratna, Elliott, Debra J., Stephen, Cole R., De Marzo, Angelo M., Gaydos, Charlotte A., Isaacs, William B., Nelson, William G.
• Format: Article
• Language: English
• ISSN: 1940-6207; 1940-6215
• DOI: 10.1158/1940-6207.PREV-11-A96

Background: Although Epstein-Barr virus (EBV), a common gamma herpesvirus known to contribute to several cancers (e.g., Burkitt's lymphoma), has been detected in prostate tissue, results from the few epidemiologic studies of EBV infection and prostate cancer have been null. One possible reason for these null findings may be that not all EBV infections contribute to prostate cancer risk. For instance, for other proposed EBV-associated conditions, such as multiple sclerosis, infections acquired later in life (e.g., in adolescence or early adulthood) when EBV infection tends to manifest as infectious mononucleosis (IM) have been found to be more important for risk than those acquired earlier in life when EBV infection is typically asymptomatic. To begin to explore the importance of later-onset EBV infections for prostate carcinogenesis, we investigated the extent of prostate pathogenesis during adult-onset IM by measuring prostate specific antigen (PSA) concentration as a marker of prostate infection, inflammation, and cell damage in adult-onset IM cases and controls with stored serum in the Department of Defense Serum repository (DoDSR). Methods: IM cases were men diagnosed with IM in 1998–2003 (n=55) and controls were a sample of men with no IM diagnoses from 1995–2006 (n=255). For each IM case, we selected two archived serum specimens from the DoDSR, one collected after their diagnosis (acute specimen, range: 1 day-3 years after diagnosis) and the first specimen collected immediately before their acute specimen (pre-acute specimen, range: 46 days-4 years before diagnosis). We also selected two specimens for each control, one collected from 1998–2003 (“acute”) and the first specimen collected immediately before their “acute” specimen (“pre-acute”). All specimens were anonymized before release from the DoDSR. We measured PSA in each of these stored specimens by the Access Hybritech PSA assay. We compared the absolute and relative change in PSA between the pre-acute and acute specimens for cases and controls using logistic regression and adjusting for age, race, and time between specimens. Results: IM cases were significantly more likely to have a large increase in PSA between their pre-acute and acute specimens than controls. This finding was observed both when PSA increase was defined as a large absolute (≥0.4 ng/mL; 9.9% versus 2.7%, p=0.033) or relative rise (≥40%; 25.2% versus 8.9%, p=0.0021). Similar results were observed when men with any infectious di