This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kawakubo, H. Articles by Maheswaran, S. Search for Related Content PubMed PubMed Citation Articles by Kawakubo, H. Articles by Maheswaran, S.

Loss of B-Cell Translocation Gene-2 in Estrogen Receptor–Positive Breast Carcinoma Is Associated with Tumor Grade and Overexpression of Cyclin D1 Protein

¹ Department of Pathology and ² Surgical Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts and ³ Department of Urology, NYU Medical Center, New York, New York

Requests for reprints: Shyamala Maheswaran, Surgical Oncology, Massachusetts General Hospital, Jackson 904, 55 Fruit Street, Boston, MA 02114. Phone: 617-724-6552; Fax: 617-726-8623; E-mail: maheswaran{at}helix.mgh.harvard.edu.

The B-cell translocation gene-2 (BTG2) is present in the nuclei of epithelial cells in many tissues, including the mammary gland where its expression is regulated during glandular proliferation and differentiation in pregnancy. In immortalized mammary epithelial cells and breast cancer cells, BTG2 protein localized predominantly to the nucleus and cytoplasm, respectively. The highly conserved domains (BTG boxes A, B, and C) were required for regulating localization, suppression of cyclin D1 and growth inhibitory function of BTG2. Expression analysis of BTG2 protein in human breast carcinoma (n = 148) revealed the loss of nuclear expression in 46% of tumors, whereas it was readily detectable in the nuclei of adjacent normal glands. Loss of nuclear BTG2 expression in estrogen receptor- (ER)–positive breast tumors correlated significantly with increased histologic grade and tumor size. Consistent with its ability to suppress cyclin D1 transcription, loss of nuclear BTG2 expression in ER-positive breast carcinomas showed a significant correlation with cyclin D1 protein overexpression, suggesting that loss of BTG2 may be a factor involved in deregulating cyclin D1 expression in human breast cancer. (Cancer Res 2006; 66(14): 7075-82)

This article has been cited by other articles:

				L. J. Donato, J. H. Suh, and N. Noy Suppression of Mammary Carcinoma Cell Growth by Retinoic Acid: the Cell Cycle Control Gene Btg2 Is a Direct Target for Retinoic Acid Receptor Signaling Cancer Res., January 15, 2007; 67(2): 609 - 615. [Abstract] [Full Text] [PDF]

				C. Yang, S. Trent, V. Ionescu-Tiba, L. Lan, T. Shioda, D. Sgroi, and E. V. Schmidt Identification of Cyclin D1- and Estrogen-Regulated Genes Contributing to Breast Carcinogenesis and Progression Cancer Res., December 15, 2006; 66(24): 11649 - 11658. [Abstract] [Full Text] [PDF]