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[Cancer Research 57, 4997-5000, November 15, 1997]
© 1997 American Association for Cancer Research
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Frequent Inactivation of PTEN/MMAC1 in Primary Prostate Cancer

Paul Cairns, Kenji Okami, Sarel Halachmi, Naomi Halachmi, Manel Esteller, James G. Herman, Jin Jen, W. B. Isaacs, G. Steven Bova and David Sidransky1

Head and Neck Cancer Research, Department of Otolaryngology [P. C., K. O., S. H., N. H., J. J., D. S.], Oncology Center [M. E., J. G. H., W. B. I., D. S.], Departments of Urology [W. B. I.] and Pathology [G. S. B.], Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Sporadic prostate carcinoma is the most common male cancer in the Western world, yet many of the major genetic events involved in the progression of this often fatal cancer remain to be elucidated. Numerous cytogenetic and allelotype studies have reported frequent loss of heterozygosity on chromosomal arm 10q in sporadic prostate cancer. Deletion mapping studies have unambiguously identified a region of chromosome 10q23 to be the minimal area of loss. A new tumor suppressor gene, PTEN/MMAC1, was isolated recently at this region of chromosome 10q23 and found to be inactivated by mutation in three prostate cancer cell lines. We screened 80 prostate tumors by microsatellite analysis and found chromosome 10q23 to be deleted in 23 cases. We then proceeded with sequence analysis of the entire PTEN/MMAC1 coding region and tested for homozygous deletion with new intragenic markers in these 23 cases with 10q23 loss of heterozygosity. The identification of the second mutational event in 10 (43%) tumors establishes PTEN/MMAC1 as a main inactivation target of 10q loss in sporadic prostate cancer.

1 To whom requests for reprints should be addressed, at Department of Otolaryngology-Head and Neck Surgery, Head and Neck Cancer Research Division, Johns Hopkins University School of Medicine, 818 Ross Research Building, 720 Rutland Avenue, Baltimore, MD 21205-2196.

Received 9/12/97. Accepted 10/ 2/97.




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