Genetic alterations in urinary bladder carcinosarcoma: Evidence of a common clonal origin

Sarel Halachmi, Angelo M. DeMarzo, Nan Haw Chow, Naomi Halachmi, Ann E. Smith, Jurgen F. Linn, Ofer Nativ, Jonathan I. Epstein, Mark P. Schoenberg, David Sidransky

Research output: Contribution to journalArticlepeer-review

61 Scopus citations


The cellular origin of carcinosarcoma of the bladder is unknown. We addressed this issue by using microsatelite analysis for loss of heterozygosity (LOH) in both the carcinomatous and sarcomatous components of 6 bladder tumors. We tested 40 microsatellite markers from 19 human chromosomes and compared the genetic alterations between the two separately isolated components. The potential relevance of the E-cadherin pathway was also evaluated by immunohistochemistry. All 6 cases revealed identical LOH on chromosomal arms 9p, 9q, 8p, and 8q, corresponding to relatively early events in bladder carcinogenesis. Discordant losses between two alleles in the remaining chromosomes, associated with progression, were seen in all tumors with a trend toward a higher incidence in the more advanced tumors (N1M1 and N1Mx). E-cadherin was strongly expressed in the carcinomatous components (5 of 6), whereas most of sarcomatous elements displayed absence of the protein product (4 of 6). These results indicate that both the carcinomatous and sarcomatous components of carcinosarcoma are derived from a common stem cell. Downregulation of E-cadherin may define one of the pathways responsible for conversion of epithelial cells to the sarcomatous phenotype. Copyright (C) 2000 S. Karger AG, Basel.

Original languageEnglish (US)
Pages (from-to)350-357
Number of pages8
JournalEuropean Urology
Issue number3
StatePublished - 2000
Externally publishedYes


  • Carcinosarcoma
  • Differentiation
  • Loss of heterozygosity
  • Microsatellite
  • Urinary bladder

ASJC Scopus subject areas

  • Urology


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