title: A novel amplification at 17q21-23 in ovarian cancer cell lines detected by comparative genomic hybridization.
abstract: OBJECTIVE
  Little is known about the molecular mechanisms involved in the pathogenesis and/or progression of ovarian cancer (OC). To investigate the genomic imbalances and identify the cancer-related genes associated with this tumor, we applied comparative genomic hybridization (CGH) in OC cell lines.
  
  
  METHODS
  Chromosomal aberrations among 17 OC cell lines were analyzed with CGH. Since novel chromosomal regions, including 17q21-23, were identified, we examined the involvement of two candidate genes, PS6K and ZNF147, mapped on this chromosomal region. We examined the status of amplification and expression by fluorescence in situ hybridization as well as by Southern blot analysis and by Northern blot analysis on two candidate genes, respectively.
  
  
  RESULTS
  All lines displayed numerous chromosomal imbalances; the most frequent losses were observed on 18q22-23 (29.4%), 13q22-34 (23.5%), 9p (17.6%), 4p11-14 (17.6%), and 11p14-15 (17.6%). The most common gains were noted at 20q12-13 (47.1%), 8q23-24 (35.2%), 5p15 (23.5%), 7q32-36 (23.5%), and 20p (23.5%). High-level gains (HLGs) were detected at 20q12-13 (four cell lines), 8q24 (two cell lines), 12p11-12 (two cell lines), and 17q21-23 (two cell lines). PS6K and ZNF147 genes were amplified in two cell lines exhibiting HLGs at 17q21-23, but not overexpressed.
  
  
  CONCLUSIONS
  Our CGH data indicate that OCs have various DNA copy number changes. Among these frequent changes, 17q21-23 may harbor another tumor-associated gene(s) responsible for OC carcinogenesis.
authors.affiliation: Department of Molecular Cytogenetics, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Watanabe
authors.forename: I
authors.initials: I
authors.lastname: Imoto
authors.forename: Y
authors.initials: Y
authors.lastname: Kosugi
authors.forename: I
authors.initials: I
authors.lastname: Ishiwata
authors.forename: S
authors.initials: S
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Takayama
authors.forename: A
authors.initials: A
authors.lastname: Sato
authors.forename: J
authors.initials: J
authors.lastname: Inazawa
mesh_terms: D002869:Chromosome Aberrations; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000235:genetics*; D005260:Female; D005784:Gene Amplification; D018628:Gene Dosage; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D009693:Nucleic Acid Hybridization; D010051:Ovarian Neoplasms / Q000235:genetics* / Q000473:pathology; D019893:Ribosomal Protein S6 Kinases / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics*; D000070584:Tripartite Motif Proteins; D014407:Tumor Cells, Cultured; D044767:Ubiquitin-Protein Ligases
chemical_list: D004268:DNA-Binding Proteins; D014157:Transcription Factors; D000070584:Tripartite Motif Proteins; C084523:TRIM25 protein, human; D044767:Ubiquitin-Protein Ligases; D019893:Ribosomal Protein S6 Kinases