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Mutational Analysis of CDKN2 (MTS1/p16^ink4) in Human Breast Carcinomas¹

Molecular Neurogenetics Unit [L. X., C. J. S., R. L. B., D. M. P., J. L. R., A. J. B., J. F. G., V. R.], Department of Pathology [D. S., S. K., D. N. L.], Molecular Neuro-Oncology Laboratory [K. U., D. N. L.], Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129

The CDKN2 gene that encodes the cell cycle regulatory protein cyclin-dependent kinase-4 inhibitor (p16) has recently been mapped to chromosome 9p21. Frequent homozygous deletions of this gene have been documented in cell lines derived from different types of tumors, including breast tumors, suggesting that CDKN2 is a tumor suppressor gene involved in a wide variety of human cancers. To determine the frequency of CDKN2 mutations in breast carcinomas, we screened 37 primary tumors and 5 established breast tumor cell lines by single-strand conformation polymorphism analysis. In addition, Southern blot analysis was performed on a set of five primary breast carcinoma samples and five breast tumor cell lines. Two of the five tumor cell lines revealed a homozygous deletion of the CDKN2 gene, but no mutations were observed in any of the primary breast carcinomas. These results suggest that the mutation of the CDKN2 gene may not be a critical genetic change in the formation of primary breast carcinoma.

¹ Supported by NIH Grant NS24279 and by grants from the U.S. Army and Bristol-Myers Squibb, Inc.

² To whom requests for reprints should be addressed, at Molecular Neurogenetics Laboratory, CNY6, Massachusetts General Hospital, Charlestown, MA 02129.

Received 6/30/94. Accepted 9/ 1/94.

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