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Mutations in PTEN Are Frequent in Endometrial Carcinoma But Rare in Other Common Gynecological Malignancies¹

Departments of Pathology [H. T., M. S. B., R. W., K. R. C., L. H. E.], Gynecology and Obstetrics [K. R. C., L. H. E.], and Oncology [K. R. C., L. H. E.], The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2196, and Departments of Pathology and Medicine, College of Physicians and Surgeons, Columbia University, New York, New York [S. B., S. I. W., J. L., R. P.]

Loss of heterozygosity of chromosome 10q has been reported in approximately 40% of endometrial carcinomas. PTEN, a candidate tumor suppressor gene located at chromosome 10q23.3, was recently identified and found to be homozygously deleted or mutated in several different types of human tumors. To determine if PTEN is a target of 10q loss of heterozygosity in carcinomas of the endometrium, we examined 32 primary endometrial carcinomas for mutations in PTEN. The tumors included the two major histopathological types of endometrial carcinoma: endometrioid (n = 26; 14 microsatellite instability (MI)-positive and 12 MI-negative) and serous (n = 6). Overall, mutations were detected in 50% of the endometrial carcinomas we analyzed. Mutations were present in 12 of 14 (86%) MI-positive and 4 of 12 (33%) MI-negative endometrioid tumors. Furthermore, mutations were found in all three histological grades of MI-positive endometrioid carcinoma. All six serous endometrial carcinomas lacked detectable mutations. To evaluate the role of PTEN in other common malignancies of the female genital tract, 12 serous ovarian carcinomas and 10 squamous cervical carcinomas were analyzed and were negative for mutations. Our results support PTEN as a tumor suppressor gene and suggest that mutations in PTEN play a significant role in the pathogenesis of the endometrioid type of endometrial carcinoma.

¹ This project was supported by funds from the Richard W. TeLinde Endowment and NIH Grants CA64466 (to K. R. C.) and CA66720 (to L. H. E.). L. H. E. is the recipient of a Passano Physician Scientist Award.

² To whom requests for reprints should be addressed, at Department of Pathology, Johns Hopkins School of Medicine, 720 Rutland Avenue, Ross Research Building Room 659, Baltimore, MD 21205.

Received 6/13/97. Accepted 7/31/97.

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				H Huang, C. Potter, W Tao, D. Li, W Brogiolo, E Hafen, H Sun, and T Xu PTEN affects cell size, cell proliferation and apoptosis during Drosophila eye development Development, January 12, 1999; 126(23): 5365 - 5372. [Abstract] [PDF]

				M. Perucho, C. R. Boland, S. N. Thibodeau, S. R. Hamilton, D. Sidransky, J. R. Eshleman, R. W. Burt, S. J. Meltzer, M. A. Rodriguez-Bigas, R. Fodde, et al. Correspondence re: C. R. Boland et al. A National Cancer Institute Workshop on Microsatellite Instability for Cancer Detection and Familial Predisposition: Development of International Criteria for the Determination of Microsatellite Instability in Colorectal Cancer. Cancer Res., 58: 5248-5257, 1998 Cancer Res., January 1, 1999; 59(1): 249 - 256. [Full Text] [PDF]

				M. Tamura, J. Gu, T. Takino, and K. M. Yamada Tumor Suppressor PTEN Inhibition of Cell Invasion, Migration, and Growth: Differential Involvement of Focal Adhesion Kinase and p130Cas Cancer Res., January 1, 1999; 59(2): 442 - 449. [Abstract] [Full Text] [PDF]

				C. C. Gurin, M. G. Federici, L. Kang, and J. Boyd Causes and Consequences of Microsatellite Instability in Endometrial Carcinoma Cancer Res., January 1, 1999; 59(2): 462 - 466. [Abstract] [Full Text] [PDF]

				M. P. Myers, I. Pass, I. H. Batty, J. Van der Kaay, J. P. Stolarov, B. A. Hemmings, M. H. Wigler, C. P. Downes, and N. K. Tonks The lipid phosphatase activity of PTEN is critical for its tumor supressor function PNAS, November 10, 1998; 95(23): 13513 - 13518. [Abstract] [Full Text] [PDF]

				A. Sakai, C. Thieblemont, A. Wellmann, E. S. Jaffe, and M. Raffeld PTEN Gene Alterations in Lymphoid Neoplasms Blood, November 1, 1998; 92(9): 3410 - 3415. [Abstract] [Full Text] [PDF]

				H. T. Lynch, M. J. Casey, T. G. Shaw, and J. F. Lynch Hereditary Factors in Gynecologic Cancer Oncologist, October 1, 1998; 3(5): 319 - 338. [Abstract] [Full Text]

				W.'e. El-Rifai, M. Sarlomo-Rikala, S. Knuutila, and M. Miettinen DNA Copy Number Changes in Development and Progression in Leiomyosarcomas of Soft Tissues Am. J. Pathol., September 1, 1998; 153(3): 985 - 990. [Abstract] [Full Text] [PDF]

				Z.-J. Wang, F. Taylor, M. Churchman, G. Norbury, and I. Tomlinson Genetic Pathways of Colorectal Carcinogenesis Rarely Involve the PTEN and LKB1 Genes Outside the Inherited Hamartoma Syndromes Am. J. Pathol., August 1, 1998; 153(2): 363 - 366. [Abstract] [Full Text] [PDF]

				Y. E. Whang, X. Wu, H. Suzuki, R. E. Reiter, C. Tran, R. L. Vessella, J. W. Said, W. B. Isaacs, and C. L. Sawyers Inactivation of the tumor suppressor PTEN/MMAC1 in advanced human prostate cancer through loss of expression PNAS, April 28, 1998; 95(9): 5246 - 5250. [Abstract] [Full Text] [PDF]

				Y. Wu, D. Dowbenko, M. T. Pisabarro, L. Dillard-Telm, H. Koeppen, and L. A. Lasky PTEN 2, a Golgi-associated Testis-specific Homologue of the PTEN Tumor Suppressor Lipid Phosphatase J. Biol. Chem., June 8, 2001; 276(24): 21745 - 21753. [Abstract] [Full Text] [PDF]

				Y. Wu, D. Dowbenko, S. Spencer, R. Laura, J. Lee, Q. Gu, and L. A. Lasky Interaction of the Tumor Suppressor PTEN/MMAC with a PDZ Domain of MAGI3, a Novel Membrane-associated Guanylate Kinase J. Biol. Chem., July 7, 2000; 275(28): 21477 - 21485. [Abstract] [Full Text] [PDF]

				S. Persad, S. Attwell, V. Gray, M. Delcommenne, A. Troussard, J. Sanghera, and S. Dedhar Inhibition of integrin-linked kinase (ILK) suppresses activation of protein kinase B/Akt and induces cell cycle arrest and apoptosis of PTEN-mutant prostate cancer cells PNAS, March 28, 2000; 97(7): 3207 - 3212. [Abstract] [Full Text] [PDF]