Cancer Research Annual Meeting 2010 EMT and Cancer Progression and Treatment
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[Cancer Research 61, 4311-4314, June 1, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Molecular Identification of Latent Precancers in Histologically Normal Endometrium1

George L. Mutter2, Tan A. Ince, Jan P. A. Baak, Gregory A. Kust, Xiao-Ping Zhou and Charis Eng

Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts 02115 [G. L. M., T. A. I., J. P. A. B., G. A. K.]; Department of Pathology, Medisch Centrum Alkmaar, Alkmaar, 1815JD the Netherlands [J. P. A. B.]; Department of Pathology, Free University, Amsterdam, 1081 HV the Netherlands [J. P. A. B.]; Clinical Cancer Genetics and Human Cancer Genetics Programs, Ohio State University Comprehensive Cancer Center, Columbus, Ohio 43210 [X-P. Z., C. E.]; and the Cancer Research Campaign Human Cancer Genetics Research Group, University of Cambridge, Cambridge, CB2 2QQ United Kingdom [C. E.]

Discovery of somatically mutated cells in human tissues has been less frequent than would be predicted by in vitro mutational rates. We analyzed the PTEN tumor suppressor gene as an early marker for endometrial carcinogenesis, and we show that 43% of histologically normal premenopausal endometria contain rare glands that fail to express PTEN protein because of mutation and/or deletion. These persist between menstrual cycles. Histopathology of PTEN-null glands is initially unremarkable, but with progression, they form distinctive high-density clusters. These data are consistent with a progression model in which initial mutation is not rate limiting.




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Copyright © 2001 by the American Association for Cancer Research.