title: CGH of microdissected Kaposi's sarcoma lesions reveals recurrent loss of chromosome Y in early and additional chromosomal changes in late tumour stages.
abstract: BACKGROUND
  It is still unclear if Kaposi's sarcoma (KS) is a monoclonal cell proliferation or a polyclonal, hyperplastic, reactive process. Reports on KS cytogenetics are few and restricted to late stage disease and cell lines.
  
  
  METHODS
  We analysed 27 KS, early and late, AIDS related (AKS) and endemic (EKS) by laser microdissection, global DNA amplification and comparative genomic hybridization (CGH).
  
  
  RESULTS
  Loss of Y chromosome was detected in 20/23 male KS, which was the only recurrent chromosomal aberration in all nine male early (patch) KS. Only one patch EKS showed in addition to the Y loss a loss of Xq. Late (nodular) AKS and EKS showed recurrent copy number changes in chromosomes 16, 17, 21, X and Y, as well as other random changes. The loss of chromosome 16, 17 and Y was confirmed by interphase fluorescence in situ hybridization (FISH) on paraffin sections. EKS showed a higher number of chromosomal abnormalities than AKS, indicating that rapid growth of AKS is less dependent on genetic changes than is EKS, possibly because of the immunosuppressed host environment in AKS.
  
  
  CONCLUSIONS
  Clonal loss of chromosome Y was detected in all early male KS, while additional chromosomal aberrations appeared during development to late KS. This increase in chromosomal abnormalities during tumour growth indicates genetic instability and the selection of survival cell clones establishing late, aggressive sarcoma growth. Our data support the view that KS (in males) develops into a clonal tumour yet initially is a hyperplastic reactive cell proliferation.
authors.affiliation: Immunopathology Laboratory, Department of Pathology and Oncology, Karolinska Institute, Stockholm, Sweden. pawan.pyakurel@ki.se
authors.forename: Pawan
authors.initials: P
authors.lastname: Pyakurel
authors.forename: Ulrike
authors.initials: U
authors.lastname: Montag
authors.forename: Esmeralda
authors.initials: E
authors.lastname: Castaños-Vélez
authors.forename: Ephata
authors.initials: E
authors.lastname: Kaaya
authors.forename: Birger
authors.initials: B
authors.lastname: Christensson
authors.forename: Holger
authors.initials: H
authors.lastname: Tönnies
authors.forename: Peter
authors.initials: P
authors.lastname: Biberfeld
authors.forename: Thomas
authors.initials: T
authors.lastname: Heiden
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000235:genetics; D002869:Chromosome Aberrations; D041321:Chromosomes, Human, X / Q000235:genetics; D041322:Chromosomes, Human, Y / Q000235:genetics*; D004273:DNA, Neoplasm / Q000235:genetics; D005260:Female; D019288:Herpesvirus 8, Human / Q000235:genetics; D006801:Humans; D017404:In Situ Hybridization, Fluorescence / Q000379:methods; D008297:Male; D042282:Microdissection / Q000379:methods; D009367:Neoplasm Staging; D021141:Nucleic Acid Amplification Techniques / Q000379:methods; D009693:Nucleic Acid Hybridization / Q000235:genetics / Q000379:methods*; D012514:Sarcoma, Kaposi / Q000235:genetics*
chemical_list: D004273:DNA, Neoplasm