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[Cancer Research 57, 5221-5225, December 1, 1997]
© 1997 American Association for Cancer Research
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MMAC1/PTEN Mutations in Primary Tumor Specimens and Tumor Cell Lines1

David H-F. Teng2, Rong Hu, Huai Lin, Thaylon Davis, Diana Iliev, Cheryl Frye, Brad Swedlund, Kipp L. Hansen, Vickie L. Vinson, Kathryn L. Gumpper, Lee Ellis, Adel El-Naggar, Marsha Frazier, Samar Jasser, Lauren A. Langford, Jeff Lee, Gordon B. Mills, Mark A. Pershouse, Raphael E. Pollack, Carmen Tornos, Patricia Troncoso, W. K. Alfred Yung, Gregory Fujii, Amy Berson, Robert Bookstein, Joseph B. Bolen, Sean V. Tavtigian and Peter A. Steck

Myriad Genetics Inc. [D. H. F. T., R. H., T. D., D. I., C. F., B. S., S. V. T.] and Myriad Genetics Laboratories Inc. [K. L. H., V. L. V., K. L. G.], Salt Lake City, Utah 84108; Department of Neuro-Oncology [H. L., S. J., M. A. P., W. K. A. Y. P. A. S.], Division of Surgery [L. E., J. L., R. E. P.], Division of Medicine [M. F., G. B. M.], and Department of Pathology [A. E. N., L. A. L., C. T., P. T.], University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030; Department of Cellular Signaling, DNAX Research Institute, Palo Alto, California 94303 [G. F., A. B., J. B. B.]; and Canji, Inc., San Diego, California 92121 [R. B.]

A candidate tumor suppressor gene, MMAC1/PTEN, located in human chromosome band 10q23, was recently identified based on sequence alterations observed in several glioma, breast, prostate, and kidney tumor specimens or cell lines. To further investigate the mutational profile of this gene in human cancers, we examined a large set of human tumor specimens and cancer cell lines of many types for 10q23 allelic losses and MMAC1 sequence alterations. Loss of heterozygosity (LOH) at the MMAC1 locus was observed in approximately one-half of the samples examined, consistent with the high frequency of 10q allelic loss reported for many cancers. Of 124 tumor specimens exhibiting LOH that have been screened for MMAC1 alterations to date, we have detected variants in 13 (~10%) of these primary tumors; the highest frequency of variants was found in glioblastoma specimens (~23%). Novel alterations identified in this gene include a missense variant in a melanoma sample and a splicing variant and a nonsense mutation in pediatric glioblastomas. Of 76 tumor cell lines prescreened for probable LOH, microsequence alterations of MMAC1 were detected in 12 (~16%) of the lines, including those derived from astrocytoma, leukemia, and melanoma tumors, as well as bladder, breast, lung, prostate, submaxillary gland, and testis carcinomas. In addition, in this set of tumor cell lines, we detected 11 (~14%) homozygous deletions that eliminated coding portions of MMAC1, a class of abnormality not detected by our methods in primary tumors. These data support the occurrence of inactivating MMAC1 alterations in multiple human cancer types. In addition, we report the discovery of a putative pseudogene of MMAC1 localized on chromosome 9.

1 This work is supported in part by NIH Grants CA56041 and CA55261 (to P. A. S.) and the generous support of the Pediatric Brain Tumor Foundation (to P. A. S., L. A. L.) and The Gilland Foundation (to W. K. A. Y.). The DNAX Research Institute is supported by Schering-Plough Corporation.

2 To whom requests for reprints should be addressed, at Myriad Genetic, Inc., 390 Wakara Way, Salt Lake City, UT 84108. Phone: (801) 584-3676; Fax: (801) 584-3650; E-mail: tengd@myriad.com.

Received 7/16/97. Accepted 10/17/97.




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