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[Cancer Research 57, 3356-3359, August 15, 1997]
© 1997 American Association for Cancer Research

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Loss of Heterozygosity at 16q24.1–q24.2 Is Significantly Associated with Metastatic and Aggressive Behavior of Prostate Cancer1

Jussi P. Elo, Päivi Härkönen, Atte P. Kyllönen, Olavi Lukkarinen, Matti Poutanen, Reijo Vihko and Pirkko Vihko2

Biocenter Oulu, WHOCCR and Department of Clinical Chemistry [J. P. E., P. H., M. P., R. V., P. V.], Surgery [O. L.], and Pathology [A. P. K.], University of Oulu, Kajaanintie 50, FIN-90220 Oulu, Finland

Several studies have indicated that in prostate cancer, frequent aberrations take place in several genomic regions. In the present study, we have analyzed allelic losses in chromosome 16 region q in 50 prostate cancer specimens of various histological grades. The most frequently deleted region was located at 16q23–16q24.2 between loci D16S504 and D16S422. The highest percentage of loss of heterozygosity (LOH) at 16q was also found within this area at loci HSD17B2 and D16S422 located at 16q24.1–q24.2. The LOH at 16q24.1–q24.2 was significantly associated with clinically aggressive behavior of the disease, metastatic disease, and higher tumor grade. Of the metastatic diseases, 83% showed LOH, whereas only 40% of the nonmetastatic diseases were found to show it. Similarly, LOH was found in 76% of the clinically aggressive diseases and in 33% of the nonaggressive diseases. The data suggest that a potentially important gene associated with prostate cancer progression is located close to 16q24.1–q24.2.

1 Supported by the Research Council for Health (project 3314) of the Academy of Finland. The Department of Clinical Chemistry is a WHO Collaborating Center for Research in Human Reproduction supported by the Ministry of Education, the Ministry of Social Affairs and Health, and the Ministry of Foreign Affairs, Finland. J. P. E. has been partly supported by the Reino Lahtikari Foundation.

2 To whom requests for reprints should be addressed. Fax: 358-8-3154451; E-mail: pvihko@whoccr.oulu.fi.

Received 1/31/97. Accepted 7/ 2/97.




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Copyright © 1997 by the American Association for Cancer Research.