title: Cytogenetic and molecular genetic characterization of immortalized human ovarian surface epithelial cell lines: consistent loss of chromosome 13 and amplification of chromosome 20.
abstract: OBJECTIVE
  This study aimed at identifying the genetic events involved in immortalization of ovarian epithelial cells, which might be important steps in ovarian carcinogenesis.
  
  
  METHODS
  The genetic profiles of five human ovarian surface epithelial (HOSE) cell lines immortalized by retroviral transfection of the human papillomavirus (HPV) E6/E7 genes were thoroughly characterized by chromosome banding and fluorescence in situ hybridization (FISH), at various passages pre- and post-crisis.
  
  
  RESULTS
  In pre-crisis, most cells had simple, non-clonal karyotypic changes. Telomere association was the commonest aberration, suggesting that tolermase dysfunction might be an important genetic event leading to cellular crisis. After immortalization post-crisis, however, the karyotypic patterns were non-random. Loss of genetic materials was a characteristic feature. The commonest numerical aberrations were -13, -14, -16, -17, -18, and +5. Among them, loss of chromosome 13 was common change observed in all lines. The only recurrent structural aberration was homogeneously staining regions (hsr) observed in three lines. FISH and combined binary ratio labeling (COBRA)-FISH showed in two cases that the hsrs were derived from chromosome 20. Clonal evolution was observed in four of the lines. In one line, hsr was the only change shared by all subclones, suggesting that it might be a primary event in cell immortalization.
  
  
  CONCLUSIONS
  The results of the present study suggested that loss of chromosome 13 and the amplification of chromosome 20 might be early genetic events involved in ovarian cell immortalization, and might be useful targets for the study of genomic aberrations in ovarian carcinogenesis.
authors.affiliation: Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China.
authors.forename: Yuesheng
authors.initials: Y
authors.lastname: Jin
authors.forename: Hao
authors.initials: H
authors.lastname: Zhang
authors.forename: Sai Wah
authors.initials: SW
authors.lastname: Tsao
authors.forename: Charlotte
authors.initials: C
authors.lastname: Jin
authors.forename: Mei
authors.initials: M
authors.lastname: Lv
authors.forename: Bodil
authors.initials: B
authors.lastname: Strömbeck
authors.forename: Joop
authors.initials: J
authors.lastname: Wiegant
authors.forename: Thomas Shek Kong
authors.initials: TS
authors.lastname: Wan
authors.forename: Po Wing
authors.initials: PW
authors.lastname: Yuen
authors.forename: Yok-Lam
authors.initials: YL
authors.lastname: Kwong
mesh_terms: D002461:Cell Line, Transformed; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D002869:Chromosome Aberrations; D002882:Chromosomes, Human, Pair 13 / Q000235:genetics*; D002890:Chromosomes, Human, Pair 20 / Q000235:genetics*; D004847:Epithelial Cells / Q000166:cytology / Q000502:physiology; D005260:Female; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D010051:Ovarian Neoplasms / Q000235:genetics*; D010053:Ovary / Q000166:cytology / Q000502:physiology / Q000648:ultrastructure*