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JNCI Journal of the National Cancer Institute 1999 91(12):1033-1039; doi:10.1093/jnci/91.12.1033
© 1999 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 91, No. 12, 1033-1039, June 16, 1999
© 1999 Oxford University Press

Cancer Surveillance Series: Interpreting Trends in Prostate Cancer—Part III: Quantifying the Link Between Population Prostate-Specific Antigen Testing and Recent Declines in Prostate Cancer Mortality

Ruth Etzioni, Julie M. Legler, Eric J. Feuer, Ray M. Merrill, Kathleen A. Cronin, Benjamin F. Hankey

Affiliations of authors: R. Etzioni, Fred Hutchinson Cancer Research Center, Seattle, WA; J. M. Legler, E. J. Feuer, K. A. Cronin, B. F. Hankey, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD; R. M. Merrill, Health Sciences Department, Brigham Young University, Provo, UT.

Correspondence to: Ruth Etzioni, Ph.D., Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., MP-665, P. O. Box 19024, Seattle, WA 98109-1024 (e-mail: retzioni{at}fhcrc.org).

BACKGROUND: The objective of this study was to investigate the circumstances under which dissemination of prostate-specific antigen (PSA) testing, beginning in 1988, could plausibly explain the declines in prostate cancer mortality observed from 1992 through 1994. METHODS: We developed a computer simulation model by use of information on population-based PSA testing patterns, cancer detection rates, average lead time (the time by which diagnosis is advanced by screening), and projected decreased risk of death associated with early diagnosis of prostate cancer through PSA testing. The model provides estimates of the number of deaths prevented by PSA testing for the 7-year period from 1988 through 1994 and projects what prostate cancer mortality for these years would have been in the absence of PSA testing. RESULTS: Results were generated by assuming a level of screening efficacy similar to that hypothesized for the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Under this assumption, the projected mortality in the absence of PSA testing continued the increasing trend observed before 1991 only when it was assumed that the mean lead time was 3 years or less. Projected mortality trends in the absence of PSA screening were not consistent with pre-1991 increasing trends for lead times of 5 years and 7 years. CONCLUSIONS: When screening is assumed to be at least as efficacious as hypothesized in the PLCO trial, it is unlikely that the entire decline in prostate cancer mortality can be explained by PSA testing based on current beliefs concerning lead time. Only very short lead times would produce a decline in mortality of the magnitude that has been observed.



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