New Ultrasensitive Assays Facilitate Studies on the Role of Human Glandular Kallikrein (hK2) as a Marker for Prostatic Disease

Abstract

Prostate cancer is the most common non-skin cancer in men, and it is an important cause of morbidity and mortality. The growth rate of prostate cancer is unusually slow. It has been estimated that the tumor starts developing at 20–30 years of age and reaches a detectable stage 30–40 years later (1). This estimate is based on the doubling time of the serum concentrations of prostate-specific antigen (PSA), ∼2 years (2), and the prevalence of high-grade prostatic intraepithelial neoplasia and microscopic cancers in prostates removed at autopsy (3)(4) in various age groups. Studies on archival serum samples from men who later developed prostate cancer have shown that the serum concentrations of PSA begin increasing 5–10 years before clinical presentation(2)(5). When serum PSA exceeds the commonly used cutoff (4 μg/L), the tumor is mostly organ-confined and potentially curable. Therefore, PSA-based screening and case finding is now increasingly used for early detection of this disease (6). However, the value of this screening is debated because the treatment causes morbidity (7) and, although recent data suggest that screening reduces prostate cancer mortality (8), the long-term effect on mortality and quality of life remains to be demonstrated. When prostate cancer is treated without curative intent, the median disease-specific survival is 17 years (5). Thus, it will not be possible to evaluate the long-term effects of screening for another 5–10 years, but it is hardly possible to reverse the trend to screen for prostate cancer until then. However, as laboratorians, we can help to reduce the negative effects of screening by developing better screening tools. Currently, the main screening tool is serum PSA, which suffers from low specificity (6). Approximately two-thirds of the increased …