title: Intensive expression of Bmi-1 is a new independent predictor of poor outcome in patients with ovarian carcinoma.
abstract: BACKGROUND
  It has been suggested that the B-cell specific moloney leukemia virus insertion site 1 (Bmi-1) gene plays an oncogenic role in several types of human cancer, but the status of Bmi-1 amplification and expression in ovarian cancer and its clinical/prognostic significance are unclear.
  
  
  METHODS
  The methods of immunohistochemistry and fluorescence in situ hybridization were utilized to examine protein expression and amplification of Bmi-1 in 30 normal ovaries, 30 ovarian cystadenomas, 40 borderline ovarian tumors and 179 ovarian carcinomas.
  
  
  RESULTS
  Intensive expression of Bmi-1 was detected in none of the normal ovaries, 3% cystadenomas, 10% borderline tumors, and 37% ovarian carcinomas, respectively. Amplification of Bmi-1 was detected in 8% of ovarian carcinomas. In ovarian carcinomas, significant positive associations were found between intensive expression of Bmi-1 and the tumors ascending histological grade, later pT/pN/pM and FIGO stages (P < 0.05). In univariate survival analysis of the ovarian carcinoma cohorts, a significant association of intensive expression of Bmi-1 with shortened patient survival (mean 49.3 months versus 100.3 months, p < 0.001) was demonstrated. Importantly, Bmi-1 expression provided significant independent prognostic parameters in multivariate analysis (p = 0.005).
  
  
  CONCLUSIONS
  These findings provide evidence that intensive expression of Bmi-1 might be important in the acquisition of an invasive and/or aggressive phenotype of ovarian carcinoma, and serve as a independent biomarker for shortened survival time of patients.
authors.affiliation: State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, No, 651, Dongfeng Road East, 510060 Guangzhou, China.
authors.forename: Guo-Fen
authors.initials: GF
authors.lastname: Yang
authors.forename: Wei-Peng
authors.initials: WP
authors.lastname: He
authors.forename: Mu-Yan
authors.initials: MY
authors.lastname: Cai
authors.forename: Li-Ru
authors.initials: LR
authors.lastname: He
authors.forename: Jun-Hang
authors.initials: JH
authors.lastname: Luo
authors.forename: Hai-Xia
authors.initials: HX
authors.lastname: Deng
authors.forename: Xin-Yuan
authors.initials: XY
authors.lastname: Guan
authors.forename: Mu-Sheng
authors.initials: MS
authors.lastname: Zeng
authors.forename: Yi-Xin
authors.initials: YX
authors.lastname: Zeng
authors.forename: Dan
authors.initials: D
authors.lastname: Xie
mesh_terms: D014408:Biomarkers, Tumor / Q000096:biosynthesis* / Q000235:genetics; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000096:biosynthesis; D005260:Female; D005784:Gene Amplification; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D008875:Middle Aged; D009687:Nuclear Proteins / Q000096:biosynthesis* / Q000235:genetics; D010051:Ovarian Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D063150:Polycomb Repressive Complex 1; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis* / Q000235:genetics; D012097:Repressor Proteins / Q000096:biosynthesis* / Q000235:genetics; D016896:Treatment Outcome; D025803:Tumor Suppressor Protein p14ARF / Q000096:biosynthesis
chemical_list: C069077:BMI1 protein, human; D014408:Biomarkers, Tumor; D019941:Cyclin-Dependent Kinase Inhibitor p16; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D012097:Repressor Proteins; D025803:Tumor Suppressor Protein p14ARF; D063150:Polycomb Repressive Complex 1