title: Models representing type I and type II human endometrial cancers: Ishikawa H and Hec50co cells.
abstract: OBJECTIVE
  Endometrial cancer models are critical to the advancement of investigation, and Ishikawa H and Hec50co cells have been used as research tools. The purpose of these studies is to verify the degree to which these commonly used cell models share the molecular characteristics of the two major in vivo endometrial cancer subtypes, I and II.
  
  
  METHODS
  The studies reported include an analysis of pathologic features, tumor suppressor mutations, detailed karyotyping, and cell cycle regulation.
  
  
  RESULTS
  Ishikawa H cells are hormone responsive and have lost PTEN expression. In addition they have lost RB1 expression due to a deletion in exon 9. Hec50co cells have lost p53 expression due to a deletion at the junction of exon 6 and intron 6-7. Compared to Ishikawa H cells, Hec50co cells harbor many more chromosomal rearrangements (29 versus seven), and the doubling time is more rapid. The percent of cells in each phase of the cell cycle is reported and linked to cell cycle regulators.
  
  
  CONCLUSIONS
  We present extensive data indicating that Ishikawa H cells are excellent models for type I endometrial cancers, and Hec50co cells faithfully replicate the molecular characteristics of type II endometrial cancers. These studies allow testing of new therapeutic regimens using appropriate cell models.
authors.affiliation: Obstetrics and Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, The Cancer Research and Treatment Center, The University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
authors.forename: Lina
authors.initials: L
authors.lastname: Albitar
authors.forename: Gavin
authors.initials: G
authors.lastname: Pickett
authors.forename: Marilee
authors.initials: M
authors.lastname: Morgan
authors.forename: Suzy
authors.initials: S
authors.lastname: Davies
authors.forename: Kimberly K
authors.initials: KK
authors.lastname: Leslie
mesh_terms: D001483:Base Sequence; D002453:Cell Cycle / Q000502:physiology; D045744:Cell Line, Tumor; D015536:Down-Regulation; D016889:Endometrial Neoplasms / Q000235:genetics* / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D016158:Genes, p53; D006801:Humans; D007621:Karyotyping; D008969:Molecular Sequence Data; D009154:Mutation; D016160:Retinoblastoma Protein / Q000235:genetics; D050720:Retinoblastoma-Like Protein p107 / Q000235:genetics; D050717:Retinoblastoma-Like Protein p130 / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics
chemical_list: C493844:RBL1 protein, human; C493837:RBL2 protein, human; D016160:Retinoblastoma Protein; D050720:Retinoblastoma-Like Protein p107; D050717:Retinoblastoma-Like Protein p130; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53