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Department of Surgery [T. M. T., J. A. M.], Human Genetics [A. C. B., T. W. G.], and Pathology [K. J. W.] and the Michigan Prostate Institute [T. M. T., K. J. W., J. A. M.], University of Michigan, Ann Arbor, Michigan 48109-0680
Utilizing tissue microdissection and PCR techniques, we have examined 35 prostate tumors paired with normal tissues from the same patients for allelic loss at 24 polymorphic loci spanning chromosome 10. Twenty-five tumors (71%) were deleted for at least one chromosome 10 locus. Of the total 35 tumors, 6 (17%) were deleted for 10p loci only, 5 (14%) for 10q loci only, and 14 (40%) were deleted for both 10p and 10q loci. The common region of deletion on 10p included loci D10S211-D10S89-D10S111. Fluorescence in situ hybridization of yeast artificial chromosome probes encompassing these loci demonstrated that the 10p region of deletion maps to 10p11.2. Losses involving 10p loci alone were most common in localized (5/14, 36%) and least common in metastatic (0/8) tumors. The common region of deletion on 10q included loci D10S219-D10S215, consistent with the major region of deletion recently defined for prostate tumors on 10q. Losses involving 10q loci alone were lowest in localized and locally invasive tumors (1/14 and 2/12, respectively) and highest in tumors metastatic to regional lymph nodes (2/8). These results suggest that 10p losses may define less invasive tumors, whereas 10q losses may play a role in the progression to more advanced tumor states in the prostate. Furthermore, this is the first report of allelic loss of a defined region on 10p potentially harboring tumor suppressor gene loci in human prostate cancer.
1 This work was supported by National Cancer Institute Grant R29 CA 06948 (J. A. M) and funds from the Michigan Prostate Institute.
2 To whom requests for reprints should be addressed, at Department of Surgery, The Michigan Prostate Institute, University of Michigan, 5510 MSRB I, 1150 West Medical Center Drive, Ann Arbor, MI 48109-0680. Phone: (313) 764-8528; Fax: (313) 763-4151.
Received 2/27/96. Accepted 4/ 2/96.
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