Suppression of invasion and peritoneal carcinomatosis of ovarian cancer cells by overexpression of AP-2α

[1]  P. Delvenne,et al.  Different mechanisms are implicated in ERBB2 gene overexpression in breast and in other cancers , 2003, British Journal of Cancer.

[2]  J. Foidart,et al.  E-Cadherin mediates MMP down-regulation in highly invasive bronchial tumor cells. , 2003, The American journal of pathology.

[3]  M. Fini,et al.  Positive influence of AP-2alpha transcription factor on cadherin gene expression and differentiation of the ocular surface. , 2003, Differentiation; research in biological diversity.

[4]  R. Weigel,et al.  Tumor Suppressor Activity of AP2α Mediated through a Direct Interaction with p53* , 2002, The Journal of Biological Chemistry.

[5]  H. Varmus,et al.  Induction of ovarian cancer by defined multiple genetic changes in a mouse model system. , 2002, Cancer cell.

[6]  J. Willson,et al.  Autocrine heregulin generates growth factor independence and blocks apoptosis in colon cancer cells , 2002, Oncogene.

[7]  Y. Hayashizaki,et al.  Cloning and Characterization of a Novel Mouse AP-2 Transcription Factor, Ap-2δ, with Unique DNA Binding and Transactivation Properties* , 2001, The Journal of Biological Chemistry.

[8]  R. Khokha,et al.  MMP Inhibitors Augment Fibroblast Adhesion through Stabilization of Focal Adhesion Contacts and Up-regulation of Cadherin Function* , 2001, The Journal of Biological Chemistry.

[9]  Jeffrey E Gershenwald,et al.  Dominant-negative transcription factor AP-2 augments SB-2 melanoma tumor growth in vivo , 2001, Oncogene.

[10]  M. Bar‐eli.  Gene regulation in melanoma progression by the AP-2 transcription factor. , 2001, Pigment cell research.

[11]  B. Davidson.  Ovarian Carcinoma and Serous Effusions. Changing Views Regarding Tumor Progression and Review of Current Literature , 2001, Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology.

[12]  I. Kobayashi,et al.  Randomized Trial of Cisplatin and Carboplatin versus Cisplatin, Vinblastine and Bleomycin in Ovarian Cancer , 2000, Gynecologic and Obstetric Investigation.

[13]  V. Kosma,et al.  Expression of transcription factor AP-2α predicts survival in epithelial ovarian cancer , 2000, British Journal of Cancer.

[14]  I. Nakashima,et al.  Protein kinase C-dependent anti-apoptotic mechanism that is associated with high sensitivity to anti-Fas antibody in ovarian cancer cell lines. , 1999, Cancer letters.

[15]  Monilola A. Olayioye,et al.  ErbB-1 and ErbB-2 Acquire Distinct Signaling Properties Dependent upon Their Dimerization Partner , 1998, Molecular and Cellular Biology.

[16]  M. Tainsky,et al.  Loss of AP‐2 results in downregulation of c‐KIT and enhancement of melanoma tumorigenicity and metastasis , 1998, The EMBO journal.

[17]  J. Gershenwald,et al.  Loss of AP-2 Results in Up-regulation ofMCAM/MUC18 and an Increase in Tumor Growth and Metastasis of Human Melanoma Cells* , 1998, The Journal of Biological Chemistry.

[18]  M. Bar‐eli.  Molecular mechanisms of melanoma metastasis , 1997, Journal of cellular physiology.

[19]  K. Zerres,et al.  Enhanced apoptotic cell death of renal epithelial cells in mice lacking transcription factor AP-2beta. , 1997, Genes & development.

[20]  D. Sheer,et al.  Chromosomal mapping of the human and mouse homologues of two new members of the AP-2 family of transcription factors. , 1996, Genomics.

[21]  A. McMahon,et al.  Neural tube, skeletal and body wall defects in mice lacking transcription factor AP-2 , 1996, Nature.

[22]  S Gaubatz,et al.  Transcriptional activation by Myc is under negative control by the transcription factor AP‐2. , 1995, The EMBO journal.

[23]  L. Williams,et al.  An alternative to SH2 domains for binding tyrosine-phosphorylated proteins. , 1994, Science.

[24]  F. Vikhanskaya,et al.  Introduction of wild-type p53 in a human ovarian cancer cell line not expressing endogenous p53. , 1994, Nucleic acids research.

[25]  M. Luther,et al.  Involvement of pp60c-src with two major signaling pathways in human breast cancer. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[26]  R. Weinberg,et al.  The pathway to signal achievement , 1993, Nature.

[27]  R. Glockshuber,et al.  An alternatively spliced mRNA from the AP-2 gene encodes a negative regulator of transcriptional activation by AP-2 , 1993, Molecular and cellular biology.

[28]  J. Ragoussis,et al.  Frequent loss of heterozygosity on chromosome 6 in human ovarian carcinoma. , 1993, British Journal of Cancer.

[29]  T. Mohandas,et al.  Localization of the gene for the DNA-binding protein AP-2 to human chromosome 6p22.3-pter. , 1991, Genomics.

[30]  R. Tjian,et al.  Analysis of the DNA-binding and activation properties of the human transcription factor AP-2. , 1991, Genes & development.

[31]  D. Slamon.  Proto-oncogenes and human cancers. , 1987, The New England journal of medicine.

[32]  F. Domann,et al.  Dominant negative interference of transcription factor AP-2 causes inhibition of ErbB-3 expression and suppresses malignant cell growth , 2004, Breast Cancer Research and Treatment.

[33]  Y. Yarden,et al.  Biochemical and clinical implications of the ErbB/HER signaling network of growth factor receptors. , 2000, Advances in cancer research.

[34]  R. Daly,et al.  Take your partners, please--signal diversification by the erbB family of receptor tyrosine kinases. , 1999, Growth factors.