Aurora-A overexpression and aneuploidy predict poor outcome in serous ovarian carcinoma.

[1]  Luis Serrano,et al.  Correlation of mRNA and protein in complex biological samples , 2009, FEBS letters.

[2]  E. Espinosa,et al.  Aurora kinases as prognostic biomarkers in ovarian carcinoma. , 2009, Human pathology.

[3]  S. Leung,et al.  Ovarian Carcinoma Subtypes Are Different Diseases: Implications for Biomarker Studies , 2008, PLoS medicine.

[4]  Liz Y. Han,et al.  Targeting Aurora Kinase with MK-0457 Inhibits Ovarian Cancer Growth , 2008, Clinical Cancer Research.

[5]  H. Saya,et al.  Aurora A overexpression induces cellular senescence in mammary gland hyperplastic tumors developed in p53-deficient mice , 2008, Oncogene.

[6]  Oliver Gautschi,et al.  Aurora Kinases as Anticancer Drug Targets , 2008, Clinical Cancer Research.

[7]  Wenlin Huang,et al.  Aurora-A, a negative prognostic marker, increases migration and decreases radiosensitivity in cancer cells. , 2007, Cancer research.

[8]  J. Ledermann,et al.  DNA Replication Licensing Factors and Aurora Kinases are Linked to Aneuploidy and Clinical Outcome in Epithelial Ovarian Carcinoma , 2007, Clinical Cancer Research.

[9]  A. Sood,et al.  Overexpression of the Centrosomal Protein Aurora-A Kinase is Associated with Poor Prognosis in Epithelial Ovarian Cancer Patients , 2007, Clinical Cancer Research.

[10]  A. Walch,et al.  Predictive Value of Aurora-A/STK15 Expression for Late Stage Epithelial Ovarian Cancer Patients Treated by Adjuvant Chemotherapy , 2007, Clinical Cancer Research.

[11]  Qing Jiang,et al.  Roles of Aurora Kinases in Mitosis and Tumorigenesis , 2007, Molecular Cancer Research.

[12]  Huan Yang,et al.  Aurora‐A induces cell survival and chemoresistance by activation of Akt through a p53‐dependent manner in ovarian cancer cells , 2006, International journal of cancer.

[13]  Gordon B Mills,et al.  Patterns of Gene Expression in Different Histotypes of Epithelial Ovarian Cancer Correlate with Those in Normal Fallopian Tube, Endometrium, and Colon , 2005, Clinical Cancer Research.

[14]  H. Joensuu,et al.  Genetic alterations and protein expression of KIT and PDGFRA in serous ovarian carcinoma , 2004, British Journal of Cancer.

[15]  H. Saya,et al.  Cre-loxP-controlled periodic Aurora-A overexpression induces mitotic abnormalities and hyperplasia in mammary glands of mouse models , 2004, Oncogene.

[16]  J. Isola,et al.  Interlaboratory Comparison of HER-2 Oncogene Amplification as Detected by Chromogenic and Fluorescence in situ Hybridization , 2004, Clinical Cancer Research.

[17]  I. Shih,et al.  Ovarian tumorigenesis: a proposed model based on morphological and molecular genetic analysis. , 2004, The American journal of pathology.

[18]  J. Gustafsson,et al.  ERBB2 amplification is superior to protein expression status in predicting patient outcome in serous ovarian carcinoma. , 2004, Gynecologic oncology.

[19]  J. Lundin,et al.  Distinct subtypes of serous ovarian carcinoma identified by p53 determination. , 2003, Gynecologic oncology.

[20]  I Vergote,et al.  Large-scale genomic instability predicts long-term outcome for women with invasive stage I ovarian cancer. , 2003, Annals of oncology : official journal of the European Society for Medical Oncology.

[21]  A. Venkitaraman,et al.  AURORA-A amplification overrides the mitotic spindle assembly checkpoint, inducing resistance to Taxol. , 2003, Cancer cell.

[22]  L. Amundadottir,et al.  Identification of phosphorylated residues that affect the activity of the mitotic kinase Aurora-A , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[23]  Young-Sun Lin,et al.  Suppression of the STK15 oncogenic activity requires a transactivation‐independent p53 function , 2002, The EMBO journal.

[24]  P. Meraldi,et al.  Aurora‐A overexpression reveals tetraploidization as a major route to centrosome amplification in p53−/− cells , 2002, The EMBO journal.

[25]  T. Seidal,et al.  Prognostic importance of DNA ploidy and p53 in early stages of epithelial ovarian carcinoma. , 2001, International journal of oncology.

[26]  H. Nevanlinna,et al.  Tenascin-C expression in invasion border of early breast cancer: a predictor of local and distant recurrence. , 1998, British Journal of Cancer.

[27]  Jian Kuang,et al.  Tumour amplified kinase STK15/BTAK induces centrosome amplification, aneuploidy and transformation , 1998, Nature Genetics.

[28]  J. Kononen,et al.  Tissue microarrays for high-throughput molecular profiling of tumor specimens , 1998, Nature Medicine.

[29]  Brian Schryver,et al.  A homologue of Drosophila aurora kinase is oncogenic and amplified in human colorectal cancers , 1998, The EMBO journal.

[30]  S. Sen,et al.  A putative serine/threonine kinase encoding gene BTAK on chromosome 20q13 is amplified and overexpressed in human breast cancer cell lines , 1997, Oncogene.

[31]  H. Risch,et al.  Differences in risk factors for epithelial ovarian cancer by histologic type. Results of a case-control study. , 1996, American journal of epidemiology.

[32]  C. Tropé,et al.  The prognostic significance of residual disease, FIGO substage, tumor histology, and grade in patients with FIGO stage III ovarian cancer. , 1995, Gynecologic oncology.

[33]  W. Sauerbrei,et al.  Cellular DNA content and survival in advanced ovarian carcinoma , 1994, Cancer.

[34]  E. Pettersen,et al.  Evaluation of deoxyribonucleic acid ploidy and S-phase fraction as prognostic parameters in advanced epithelial ovarian carcinoma: A prospective study , 1994 .

[35]  V. Abeler,et al.  Analysis of prognostic factors in stage I epithelial ovarian carcinoma: importance of degree of differentiation and deoxyribonucleic acid ploidy in predicting relapse. , 1993, American journal of obstetrics and gynecology.