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© Oxford University Press 2007.
MEMO TO THE MEDIA |
Press Release
PSA Is Poor Predictor of Lethal Prostate Cancer
jncimedia{at}oxfordjournals.org
301-841-1287
Journal of the National Cancer Institute
The amount of prostate-specific antigen (PSA) in a man's bloodstream at the time of his prostate cancer diagnosis or its rate of change over the course of the disease does not adequately predict lethal prostate cancer, according to a study in the April 4 Journal of the National Cancer Institute.
Although men with untreated localized prostate cancer have high long-term survival rates, many patients undergo treatment anyway. In order to avoid unnecessary treatment, researchers want to identify methods to determine which patients will develop lethal prostate cancer. The rate of increase of PSA—a protein produced by the prostate—before prostate cancer treatment has been associated with the patient's prognosis, which suggests that early measurements of PSA may predict the behavior of the tumor.
To assess the accuracy of using PSA to predict prostate cancer outcome, Katja Fall, M.D., Ph.D., of the Karolinska Institute in Stockholm, and colleagues analyzed the rate of change of PSA levels in 267 men from Sweden, Finland, and Iceland who were diagnosed with early localized prostate cancer between 1989 and 1999. The researchers recorded the PSA levels for the first two years after diagnosis to capture the patients’ early PSA patterns. The men in the study received no curative treatment for the first two years but were closely watched for signs of progression, which is called watchful waiting.
At the end of the follow-up in December 2003, 34 patients had died from prostate cancer, and 18 had developed metastatic prostate cancer but were still alive. Although initial PSA values and the rate of change were associated with later development of lethal prostate cancer, they were not accurate enough to predict lethal cancer.
"We conclude that PSA measurement is associated with prostate cancer prognosis and continues to be an important monitoring tool," the authors write. "However, early PSA characteristics perform poorly in distinguishing those who develop a lethal prostate cancer from those at low or no risk of disease progression. Therefore, better decision tools are needed for active monitoring of patients with early disease."
In an accompanying editorial, Dipen Parekh, M.D., of the University of Texas Health Science Center at San Antonio, and colleagues compared the results of this new study with their own work and found consistent results regarding PSA, as well as other measures that were related to prostate cancer risk. "These data demand that clinical trials commence now to examine surveillance strategies to help patients and their physicians identify and treat tumors that will otherwise be life threatening and to carefully follow those that will not. Our limited health care resources and the quality of life of an enormous number of men will benefit from this for decades to come," the authors write.
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Contact:
- Article: Katarina Sternudd, press officer, Karolinska Institute, +46 8 524 838 95, katarina.sternudd{at}ki.se
- Editorial: Dipen Parekh, University of Texas Health Science Center, (210) 567-5643, parekhd{at}uthscsa.edu
Citation:
- Article: Fall K, Garmo H, Andrén O, Axelson AB, Adolfsson J, Adami HO, Johansson JE, Holmberg L. Prostate-Specific Antigen Levels as a Predictor of Lethal Prostate Cancer. J Natl Cancer Inst 2007; 99: 526–532
- Editorial: Parekh DJ, Ankerst DP, Thompson IM. Prostate-Specific Antigen Levels, Prostate-Specific Antigen Kinetics, and Prostate Cancer Prognosis: A Tocsin Calling for Prospective Studies. J Natl Cancer Inst 2007; 99: 496–497
Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jnci.oxfordjournals.org/.
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Del.icio.us What's this?
J Natl Cancer Inst 2007 99: 496-497.
J Natl Cancer Inst 2007 99: 526-532.
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