title: Recurrent and multiple bladder tumors show conserved expression profiles.
abstract: BACKGROUND
  Urothelial carcinomas originate from the epithelial cells of the inner lining of the bladder and may appear as single or as multiple synchronous tumors. Patients with urothelial carcinomas frequently show recurrences after treatment making follow-up necessary. The leading hypothesis explaining the origin of meta- and synchronous tumors assumes a monoclonal origin. However, the genetic relationship among consecutive tumors has been shown to be complex in as much as the genetic evolution does not adhere to the chronological appearance of the metachronous tumors. Consequently, genetically less evolved tumors may appear chronologically later than genetically related but more evolved tumors.
  
  
  METHODS
  Forty-nine meta- or synchronous urothelial tumors from 22 patients were analyzed using expression profiling, conventional CGH, LOH, and mutation analyses.
  
  
  RESULTS
  We show by CGH that partial chromosomal losses in the initial tumors may not be present in the recurring tumors, by LOH that different haplotypes may be lost and that detected regions of LOH may be smaller in recurring tumors, and that mutations present in the initial tumor may not be present in the recurring ones. In contrast we show that despite apparent genomic differences, the recurrent and multiple bladder tumors from the same patients display remarkably similar expression profiles.
  
  
  CONCLUSIONS
  Our findings show that even though the vast majority of the analyzed meta- and synchronous tumors from the same patients are not likely to have originated directly from the preceding tumor they still show remarkably similar expressions profiles. The presented data suggests that an expression profile is established early in tumor development and that this profile is stable and maintained in recurring tumors.
authors.affiliation: Department of Clinical Genetics, Lund University Hospital, Lund, Sweden. david.lindgren@med.lu.se
authors.forename: David
authors.initials: D
authors.lastname: Lindgren
authors.forename: Sigurdur
authors.initials: S
authors.lastname: Gudjonsson
authors.forename: Kowan Ja
authors.initials: KJ
authors.lastname: Jee
authors.forename: Fredrik
authors.initials: F
authors.lastname: Liedberg
authors.forename: Sonja
authors.initials: S
authors.lastname: Aits
authors.forename: Anna
authors.initials: A
authors.lastname: Andersson
authors.forename: Gunilla
authors.initials: G
authors.lastname: Chebil
authors.forename: Ake
authors.initials: A
authors.lastname: Borg
authors.forename: Sakari
authors.initials: S
authors.lastname: Knuutila
authors.forename: Thoas
authors.initials: T
authors.lastname: Fioretos
authors.forename: Wiking
authors.initials: W
authors.lastname: Månsson
authors.forename: Mattias
authors.initials: M
authors.lastname: Höglund
mesh_terms: D002277:Carcinoma / Q000235:genetics* / Q000473:pathology; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D004252:DNA Mutational Analysis; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D009364:Neoplasm Recurrence, Local / Q000235:genetics*; D009367:Neoplasm Staging; D009378:Neoplasms, Multiple Primary / Q000235:genetics*; D020411:Oligonucleotide Array Sequence Analysis; D017354:Point Mutation / Q000235:genetics; D051498:Receptor, Fibroblast Growth Factor, Type 3 / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D001749:Urinary Bladder Neoplasms / Q000235:genetics* / Q000473:pathology
chemical_list: C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; C496365:FGFR3 protein, human; D051498:Receptor, Fibroblast Growth Factor, Type 3