PMID- 16954721
OWN - NLM
STAT- MEDLINE
DCOM- 20070205
LR  - 20060906
IS  - 0269-9370 (Print)
IS  - 0269-9370 (Linking)
VI  - 20
IP  - 14
DP  - 2006 Sep 11
TI  - CGH of microdissected Kaposi's sarcoma lesions reveals recurrent loss of 
      chromosome Y in early and additional chromosomal changes in late tumour stages.
PG  - 1805-12
AB  - 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. METHOD: 
      We analysed 27 KS, early and late, AIDS related (AKS) and endemic (EKS) by laser 
      microdissection, global DNA amplification and comparative genomic hybridization 
      (CGH). RESULT: 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. CONCLUSION: 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.
FAU - Pyakurel, Pawan
AU  - Pyakurel P
AD  - Immunopathology Laboratory, Department of Pathology and Oncology, Karolinska 
      Institute, Stockholm, Sweden. pawan.pyakurel@ki.se
FAU - Montag, Ulrike
AU  - Montag U
FAU - Castanos-Velez, Esmeralda
AU  - Castanos-Velez E
FAU - Kaaya, Ephata
AU  - Kaaya E
FAU - Christensson, Birger
AU  - Christensson B
FAU - Tonnies, Holger
AU  - Tonnies H
FAU - Biberfeld, Peter
AU  - Biberfeld P
FAU - Heiden, Thomas
AU  - Heiden T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (DNA, Neoplasm)
SB  - IM
MH  - Acquired Immunodeficiency Syndrome/genetics
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, X/genetics
MH  - Chromosomes, Human, Y/*genetics
MH  - DNA, Neoplasm/genetics
MH  - Female
MH  - Herpesvirus 8, Human/genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence/methods
MH  - Male
MH  - Microdissection/methods
MH  - Neoplasm Staging
MH  - Nucleic Acid Amplification Techniques/methods
MH  - Nucleic Acid Hybridization/genetics/*methods
MH  - Sarcoma, Kaposi/*genetics
EDAT- 2006/09/07 09:00
MHDA- 2007/02/06 09:00
CRDT- 2006/09/07 09:00
PHST- 2006/09/07 09:00 [pubmed]
PHST- 2007/02/06 09:00 [medline]
PHST- 2006/09/07 09:00 [entrez]
AID - 00002030-200609110-00003 [pii]
AID - 10.1097/01.aids.0000244199.72887.3d [doi]
PST - ppublish
SO  - AIDS. 2006 Sep 11;20(14):1805-12. doi: 10.1097/01.aids.0000244199.72887.3d.