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Urologic Cancer Research Laboratory, Kenneth Norris Jr. Comprehensive Cancer Center, University of Southern California School of Medicine, Los Angeles, California 90033 [M. G-Z., Y. C. T., C. H. S., N. M., P. W. N., P. A. J.]; Department of Otolaryngology-Head and Neck Surgery, the Johns Hopkins University, Baltimore, Maryland 21205 [J. M. R., K. T., D. S.]; Department of Urology, Herlev Hospital, University of Copenhagen, Herlev, Denmark [G. G. H., T. H., K. S.]; and Laboratory of Cancer Biology and Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115 [I. C. S.]
3 To whom requests for reprints should be addressed, at the Kenneth Norris Jr. Comprehensive Cancer Center, University of Southern California, 1441 East Lake Ave. Los Angeles, CA 90033-0800.
Somatic instability at microsatellite repeats was detected in 6 of 200 transitional cell carcinomas of the bladder. Instabilities were apparent as changes in (GT)n repeat lengths on human chromosome 9 for four tumors and as alterations in a (CAG)n repeat in the androgen receptor gene on the X chromosome for three tumors. Single locus alterations were detected in three tumors, while three other tumors revealed changes in two or more loci. In one tumor we found microsatellite instability in all five loci analyzed on chromosome 9. The alterations detected were either minor 2-base pair changes or larger (>2 base pairs) alterations in repeat length. All six tumors were low stage (Ta–T1), suggesting that these alterations can occur early in bladder tumorigenesis.
1 Supported by USPHS Grant R35 CA49758 from the National Cancer Institute, and a Collaborative Research agreement with Oncor, Inc., Gaithersburg, MD.
2 Recipient of a fellowship from The Government of Navarra, Spain.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 8/30/93. Accepted 10/18/93.
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