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| Research article summary (published 4 Oct 2009): |
Somatic single hits inactivate the X-linked tumor suppressor FOXP3 in the prostate.
Full Abstract
Despite clear epidemiological and genetic evidence for X-linked prostate cancer risk, all prostate cancer genes identified are autosomal. Here, we report somatic inactivating mutations and deletion of the X-linked FOXP3 gene residing at Xp11.23 in human prostate cancer. Lineage-specific ablation of FoxP3 in the mouse prostate epithelial cells leads to prostate hyperplasia and prostate intraepithelial neoplasia. In both normal and malignant prostate tissues, FOXP3 is both necessary and sufficient to transcriptionally repress cMYC, the most commonly overexpressed oncogene in prostate cancer as well as among the aggregates of other cancers. FOXP3 is an X-linked prostate tumor suppressor in the male. Because the male has only one X chromosome, our data represent a paradigm of "single genetic hit" inactivation-mediated carcinogenesis.
Author information
Author/s: Wang, Lizhong (L); Liu, Runhua (R); Li, Weiquan (W); Chen, Chong (C); Katoh, Hiroto (H); Chen, Guo-Yun (GY); McNally, Beth (B); Lin, Lin (L); Zhou, Penghui (P); Zuo, Tao (T); Cooney, Kathleen A (KA); Liu, Yang (Y); Zheng, Pan (P);
Affiliation: Division of Immunotherapy, Department of Surgery, University of Michigan School of Medicine and Cancer Center, Ann Arbor, MI 48109, USA.
Journal and publication information
Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
Journal: Cancer cell (Cancer Cell), published in United States. (Language: eng)
Reference: 2009-Oct; vol 16 (issue 4) : pp 336-46
Dates: Created 2009/10/05; Completed 2009/10/15;
PMID: 19800578, status: MEDLINE (last retrieval date: 10/15/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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