title: Molecular evidence for the independent origin of extra-ovarian papillary serous tumors of low malignant potential.
abstract: BACKGROUND
  Molecular data suggest that peritoneal tumors in women with advanced-stage ovarian papillary serous adenocarcinoma are monoclonal in origin. Whether the same is true for ovarian tumors of low malignant potential is not known. We compared peritoneal and ovarian tumors from women with advanced-stage ovarian papillary serous tumors of low malignant potential to determine whether the peritoneal tumors arose from the same clone as the ovarian tumors.
  
  
  METHODS
  We studied the clonality of 73 peritoneal and ovarian tumors from 18 women with advanced-stage ovarian papillary serous tumors of low malignant potential. Formalin-fixed, paraffin-embedded tumors and representative normal tissues were sectioned and stained with hematoxylin-eosin, representative sections from separate tumors were manually microdissected, genomic DNA was extracted from the microdissected tumors, and the polymerase chain reaction was used to amplify a CAG polymorphic site in the human androgen receptor locus on the X chromosome to determine the inactivation pattern of the X chromosome and the clonality of the tumors.
  
  
  RESULTS
  The pattern of X-chromosome inactivation could be determined from the tumors of 13 of 18 patients. Of the 13 patients, seven (54%) had nonrandom inactivation of the X chromosome, and six of the seven had different inactivation patterns in the peritoneal and ovarian tumors. Three of these patients also had different patterns of nonrandom X-chromosome inactivation in tumors from each ovary. The remaining six patients had random patterns of X-chromosome inactivation in the peritoneal and ovarian tumors.
  
  
  CONCLUSIONS
  Our data suggest that peritoneal and ovarian tumors of low malignant potential arise independently.
authors.affiliation: Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, USA.
authors.forename: J
authors.initials: J
authors.lastname: Gu
authors.forename: L M
authors.initials: LM
authors.lastname: Roth
authors.forename: C
authors.initials: C
authors.lastname: Younger
authors.forename: H
authors.initials: H
authors.lastname: Michael
authors.forename: F W
authors.initials: FW
authors.lastname: Abdul-Karim
authors.forename: S
authors.initials: S
authors.lastname: Zhang
authors.forename: T M
authors.initials: TM
authors.lastname: Ulbright
authors.forename: J N
authors.initials: JN
authors.lastname: Eble
authors.forename: L
authors.initials: L
authors.lastname: Cheng
mesh_terms: D000231:Adenocarcinoma, Papillary / Q000235:genetics* / Q000556:secondary; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D004262:DNA Restriction Enzymes / Q000235:genetics; D004273:DNA, Neoplasm / Q000032:analysis; D005260:Female; D006801:Humans; D008745:Methylation; D008875:Middle Aged; D010051:Ovarian Neoplasms / Q000235:genetics* / Q000473:pathology*; D010534:Peritoneal Neoplasms / Q000235:genetics* / Q000556:secondary; D016133:Polymerase Chain Reaction; D012729:Sex Chromosome Aberrations / Q000235:genetics; D019680:Trinucleotide Repeat Expansion; D014960:X Chromosome / Q000235:genetics*
chemical_list: D004273:DNA, Neoplasm; D004262:DNA Restriction Enzymes