Loss of the 14-3-3σ tumor suppressor is a critical event in ErbB2-mediated tumor progression.
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W. Muller | D. Zuo | C. Ling | Vi-Minh-Tri Su
[1] W. Muller,et al. A novel role for 14-3-3sigma in regulating epithelial cell polarity. , 2010, Genes & development.
[2] M. Hung,et al. 14-3-3zeta Cooperates with ErbB2 to promote ductal carcinoma in situ progression to invasive breast cancer by inducing epithelial-mesenchymal transition. , 2009, Cancer cell.
[3] U. Rapp,et al. Regulation of RAF Activity by 14-3-3 Proteins , 2009, Journal of Biological Chemistry.
[4] Z. Xuan,et al. Deregulation of Scribble Promotes Mammary Tumorigenesis and Reveals a Role for Cell Polarity in Carcinoma , 2008, Cell.
[5] T. Pawson,et al. ShcA signalling is essential for tumour progression in mouse models of human breast cancer , 2008, The EMBO journal.
[6] Stephen T. Brown,et al. An EGR2/CITED1 Transcription Factor Complex and the 14-3-3σ Tumor Suppressor Are Involved in Regulating ErbB2 Expression in a Transgenic-Mouse Model of Human Breast Cancer , 2007, Molecular and Cellular Biology.
[7] Wen-Lin Kuo,et al. A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes. , 2006, Cancer cell.
[8] Marissa E. Nolan,et al. Par6–aPKC uncouples ErbB2 induced disruption of polarized epithelial organization from proliferation control , 2006, Nature Cell Biology.
[9] D. Lodygin,et al. Epigenetic silencing of 14-3-3sigma in cancer. , 2006, Seminars in Cancer Biology.
[10] I. Verma,et al. Identification of 14-3-3sigma mutation causing cutaneous abnormality in repeated-epilation mutant mouse. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[11] J. Gray,et al. Copy number aberrations in mouse breast tumors reveal loci and genes important in tumorigenic receptor tyrosine kinase signaling. , 2005, Cancer research.
[12] L. Siracusa,et al. A mutation in stratifin is responsible for the repeated epilation (Er) phenotype in mice , 2005, Nature Genetics.
[13] John R Yates,et al. Targeted Proteomic Analysis of 14-3-3ς, a p53 Effector Commonly Silenced in Cancer*S , 2005, Molecular & Cellular Proteomics.
[14] D. Lodygin,et al. The role of epigenetic inactivation of 14-3-3σ in human cancer , 2005, Cell Research.
[15] H. Yoshida,et al. Frequent downregulation of 14-3-3 σ protein and hypermethylation of 14-3-3 σ gene in salivary gland adenoid cystic carcinoma , 2004, British Journal of Cancer.
[16] Hye Kyong Kweon,et al. Phosphorylation-Dependent Binding of 14-3-3 to the Polarity Protein Par3 Regulates Cell Polarity in Mammalian Epithelia , 2003, Current Biology.
[17] Satoshi Inoue,et al. Efp targets 14-3-3σ for proteolysis and promotes breast tumour growth , 2002, Nature.
[18] T. Ried,et al. Centrosome abnormalities, recurring deletions of chromosome 4, and genomic amplification of HER2/neu define mouse mammary gland adenocarcinomas induced by mutant HER2/neu , 2002, Oncogene.
[19] T. Pandita,et al. High frequency of hypermethylation at the 14-3-3 sigma locus leads to gene silencing in breast cancer. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[20] F. Leenders,et al. Mammary gland specific hEGF receptor transgene expression induces neoplasia and inhibits differentiation , 2000, Oncogene.
[21] M. Rudnicki,et al. Amplification of the neu/erbB-2 oncogene in a mouse model of mammary tumorigenesis. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[22] K. Kinzler,et al. 14-3-3σ is required to prevent mitotic catastrophe after DNA damage , 1999, Nature.
[23] R. Cardiff,et al. Elevated expression of activated forms of Neu/ErbB‐2 and ErbB‐3 are involved in the induction of mammary tumors in transgenic mice: implications for human breast cancer , 1999, The EMBO journal.
[24] S. Bull,et al. neu/erbB-2 amplification identifies a poor-prognosis group of women with node-negative breast cancer. Toronto Breast Cancer Study Group. , 1998, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[25] X. Cullere,et al. Serine 257 Phosphorylation Regulates Association of Polyomavirus Middle T Antigen with 14-3-3 Proteins , 1998, Journal of Virology.
[26] K. Kinzler,et al. 14-3-3σ Is a p53-Regulated Inhibitor of G2/M Progression , 1997 .
[27] R. Cardiff,et al. Activated neu Induces Rapid Tumor Progression (*) , 1996, The Journal of Biological Chemistry.
[28] R. Palmiter,et al. Inhibition of mammary gland involution is associated with transforming growth factor alpha but not c-myc-induced tumorigenesis in transgenic mice. , 1995, Cancer research.
[29] C. Croce,et al. Detection and cloning of a common region of loss of heterozygosity at chromosome 1p in breast cancer. , 1995, Cancer research.
[30] E. Valverius,et al. Complementary DNA cloning of a novel epithelial cell marker protein, HME1, that may be down-regulated in neoplastic mammary cells. , 1992, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[31] A. Villa,et al. Early and multifocal tumors in breast, salivary, harderian and epididymal tissues developed in MMTY-Neu transgenic mice. , 1992, Cancer letters.
[32] O. Garson,et al. Rearrangement of chromosome 1p in breast cancer correlates with poor prognostic features. , 1992, British Journal of Cancer.
[33] G. Stenman,et al. Expression of the ERBB2 protein in benign and malignant salivary gland tumors , 1991, Genes, chromosomes & cancer.
[34] N. Kernohan,et al. Expression of c‐erbB‐2 oncoprotein in salivary gland tumours: An immunohistochemical study , 1991, The Journal of pathology.
[35] R. Palmiter,et al. Overexpression of TGFα in transgenic mice: Induction of epithelial hyperplasia, pancreatic metaplasia, and carcinoma of the breast , 1990, Cell.
[36] B. Hogan,et al. Development of mammary hyperplasia and neoplasia in MMTV-TGFα transgenic mice , 1990, Cell.
[37] N. Lemoine,et al. Absence of activating transmembrane mutations in the c-erbB-2 proto-oncogene in human breast cancer. , 1990, Oncogene.
[38] P. Jolicoeur,et al. Stochastic appearance of mammary tumors in transgenic mice carrying the MMTV/c-neu oncogene , 1989, Cell.
[39] W Godolphin,et al. Studies of the HER-2/neu proto-oncogene in human breast and ovarian cancer. , 1989, Science.
[40] P. Leder,et al. Single-step induction of mammary adenocarcinoma in transgenic mice bearing the activated c-neu oncogene , 1988, Cell.
[41] P. Leder,et al. Coexpression of MMTV/v-Ha-ras and MMTV/c-myc genes in transgenic mice: Synergistic action of oncogenes in vivo , 1987, Cell.
[42] K. Semba,et al. A v-erbB-related protooncogene, c-erbB-2, is distinct from the c-erbB-1/epidermal growth factor-receptor gene and is amplified in a human salivary gland adenocarcinoma. , 1985, Proceedings of the National Academy of Sciences of the United States of America.
[43] F. Révillion,et al. Proteomic analysis reveals that 14-3-3σ is down-regulated in human breast cancer cells , 2001 .
[44] P. Ravdin. neu/erbB-2 amplification identifies a poor-prognosis group of women with node-negative breast cancer , 1999 .
[45] A. Knudson. Introduction to the genetics of primary renal tumors in children. , 1993, Medical and pediatric oncology.
[46] B. Hogan,et al. Development of mammary hyperplasia and neoplasia in MMTV-TGF alpha transgenic mice. , 1990, Cell.
[47] D. Weiner,et al. Expression pattern of the neu (NGL) gene-encoded growth factor receptor protein (p185neu) in normal and transformed epithelial tissues of the digestive tract. , 1989, Oncogene.
[48] W. McGuire,et al. Human breast cancer: correlation of relapse and survival with amplification of the HER-2/neu oncogene. , 1987, Science.
[49] K. Semba. A v-erbB-related protooncogene, c-erb-B-1/epidermal growth factor-receptor gene and is amplified in a human salivary gland adenocarcinoma , 1985 .