Clinical Chemistry
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Clinical Chemistry 44: 72-77, 1998;
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(Clinical Chemistry. 1998;44:72-77.)
© 1998 American Association for Clinical Chemistry, Inc.

Molecular Pathology and Genetics

Exon 5 of the p53 gene is a target for deletions in ovarian cancer

Katerina Angelopoulou1,2, Michael A. Levesque1,2, Dionyssios Katsaros3, Rob Shipman4, and Eleftherios P. Diamandis1,2,1

1 Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, 600 University Ave., Toronto, ON, Canada M5G 1X5.

2 Department of Laboratory Medicine and Pathobiology, University of Toronto, 100 College St., Toronto, ON, Canada M5G 1L5.

3 Department of Gynecologic Oncology, Institute of Obstetrics and Gynecology, University of Turin, Turin, Italy.

4 Visible Genetics Inc., 700 Bay St., Ste. #1000, Box 333, Toronto, ON, Canada M5G 1Z9.

Missense point mutations, leading to inactivation of the p53 tumor suppressor gene product, are currently the most frequent alterations in human cancer. Little, however, is known about small intragenic deletions or insertions occurring in this locus of chromosome 17. We have analyzed 56 primary ovarian tumors for the presence of such abnormalities. The analysis was based on multiplex PCR amplification of exons 1 through 11 of the p53 gene and fragment analysis of the generated PCR products. Mutations were detected in 14% (8 of 56) of the tumors. Deletions were much more prevalent than insertions (seven vs one). Six of the deletions and the insertion affected exon 5, and the other deletion was in exon 7. Two deletions and the insertion did not disrupt the reading frame; the protein product was expressed in the tumor at high concentrations in all three cases. The other five deletions generated a frameshift, which is predicted to result in the production of a truncated protein product. In the case of the deletions, a 2–5-bp repeat was present close to the detected deletion, whereas the insertion duplicated the sequence immediately upstream of the insertion site. Overall our findings indicate that small intragenic p53 deletions/insertions are not rare events in ovarian cancer, and that p53 exon 5 is the target in the vast majority (88%) of the cases.




The following articles in journals at HighWire Press have cited this article:


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 Clin. Cancer Res.Home page
A. Reles, W. H. Wen, A. Schmider, C. Gee, I. B. Runnebaum, U. Kilian, L. A. Jones, A. El-Naggar, C. Minguillon, I. Schonborn, et al.
Correlation of p53 Mutations with Resistance to Platinum-based Chemotherapy and Shortened Survival in Ovarian Cancer
Clin. Cancer Res., October 1, 2001; 7(10): 2984 - 2997.
[Abstract] [Full Text] [PDF]


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