title: Overexpression of polycomb protein BMI-1 in human specimens of breast, ovarian, endometrial and cervical cancer.
abstract: BACKGROUND
  The polycomb group (PcG) proteins form chromatin-modifying complexes that are commonly deregulated in cancer. The PcG protein BMI-I is overexpressed by various tumours and thus may contribute to malignant transformation. The current study investigated the expression of BMI-I in human specimens of breast, ovarian, endometrial and cervical cancer.
  
  
  METHODS
  Expression of BMI-I was evaluated in human ovarian cancer samples by Western blot analysis and immunohistochemistry (IHC) and compared to healthy ovarian tissue. BMI-I expression in human specimens of breast, endometrial and cervical cancer was evaluated by IHC and then compared with the respective benign tissues.
  
  
  RESULTS
  BMI-I was significantly (p<0.05) overexpressed in human breast, ovarian, endometrial and cervical cancer specimens as compared to benign controls. BMI-I expression was also more pronounced in the ovarian cancer samples as demonstrated by Western blot analysis. In human breast cancer samples, BMI-I expression was most pronounced in the invasion front of the tumour.
  
  
  CONCLUSIONS
  The current study showed for the first time that the BMI-I protein is significantly overexpressed in ovarian, endometrial and cervical cancer and may thus be a potential target for novel antitumor therapies.
authors.affiliation: Department of Gynecology and Obstetrics, Medical University of Würzburg, Würzburg, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Honig
authors.forename: C
authors.initials: C
authors.lastname: Weidler
authors.forename: S
authors.initials: S
authors.lastname: Häusler
authors.forename: M
authors.initials: M
authors.lastname: Krockenberger
authors.forename: S
authors.initials: S
authors.lastname: Buchholz
authors.forename: F
authors.initials: F
authors.lastname: Köster
authors.forename: S E
authors.initials: SE
authors.lastname: Segerer
authors.forename: J
authors.initials: J
authors.lastname: Dietl
authors.forename: J B
authors.initials: JB
authors.lastname: Engel
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D001943:Breast Neoplasms / Q000378:metabolism*; D002454:Cell Differentiation; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016889:Endometrial Neoplasms / Q000378:metabolism*; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D019394:Ki-67 Antigen / Q000096:biosynthesis; D009363:Neoplasm Proteins / Q000378:metabolism; D009687:Nuclear Proteins / Q000096:biosynthesis* / Q000502:physiology*; D010051:Ovarian Neoplasms / Q000378:metabolism*; D010641:Phenotype; D063150:Polycomb Repressive Complex 1; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis* / Q000502:physiology*; D012097:Repressor Proteins / Q000096:biosynthesis* / Q000502:physiology*; D002583:Uterine Cervical Neoplasms / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; C069077:BMI1 protein, human; C000614131:CDKN2A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D012097:Repressor Proteins; D063150:Polycomb Repressive Complex 1