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Imperial Cancer Research Fund, Clare Hall Laboratories, South Mimms, Potters Bar, Herts EN6 3LD, United Kingdom [I. C. G., N. K. S.]; Department of Surgery, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2TH, United Kingdom [S. M. A. P., J. P. N.]; Central Manchester Healthcare National Health Service Trust, St. Mary's Hospital for Women and Children, Manchester M13 OJH, United Kingdom [S. J. L.]; and Genethon, 1 rue de l'Internationale, 91000 Evry, France [J. W.]
Loss of the chromosomal region 10q23–25 is a frequent event in the progression of prostate adenocarcinoma. A candidate tumor suppressor gene from this region, Mxi1 at 10q25, has recently been shown to be mutated in a small number of prostate tumors. To more strictly define those regions of 10q loss that are likely to be involved in tumor advancement, we have constructed a detailed deletion map spanning 10q23–25 that incorporates Mxi1. Sixty-two % (23 of 37) of tumors analyzed exhibited some degree of 10q23–25 loss. Our data suggest the presence of a prostate tumor suppressor gene(s) near the 10q23–24 boundary, which was deleted in the overwhelming majority (22 of 23) of tumors showing loss. In contrast, specific loss of Mxi1, as opposed to loss of other 10q23–25 regions or of the entire region, was observed in only 1 of 23 tumors and was accompanied by loss of markers at the 10q23–24 boundary. Furthermore, we failed to detect any mutations in Mxi1 in those tumors showing Mxi1-associated marker loss by either single-strand conformation polymorphism analysis or direct DNA sequencing.
1 Supported by the Imperial Cancer Research Fund.
2 To whom requests for reprints should be addressed.
Received 7/31/95. Accepted 9/20/95.
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