Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
|
pubmed:dateCreated |
1999-5-24
|
pubmed:abstractText |
We used comparative genomic hybridization (CGH) to evaluate DNA sequence copy number changes in 67 synovial sarcomas of both monophasic and biphasic histological subtypes. Changes (mean among aberrant cases: 4.7 aberrations/tumor; range: 1-17), affecting most often entire chromosomes or chromosome arms, were detected in 37 sarcomas (55%). Gains and losses were distributed equally, but different chromosomes were affected with variable frequencies. The most frequent aberrations, each detected in 9-11 of 67 tumors, were gain of 8q and gain at 12q (12q14-15 and 12q23-qter), loss of 13q21-31, and loss of 3p. Other frequent changes (in 7 or 8 cases) included gains at 2p, 1q24-31, and 17q22-qter, and losses at 3cen-q23 and 10q21. High-level amplifications were seen in 7 cases. A total of 16 regions were detected. Two of them, 8p12-qter and 21q21-qter, seen in 4 and 2 tumors, respectively, were recurrent. No aberrations specific to histological subtype were identified. However, genetic changes in the monophasic tumors were more complex and numerous (mean among aberrant cases: 5.3 aberrations/tumor; range: 1-17) than in the biphasic tumors (mean: 2.5 aberrations/tumor; range: 1-5), and high-level amplifications occurred more frequently. All but 1 of the sarcomas showing high-level amplification were of the monophasic subtype. These findings may reflect differences in the pathogenesis and biological behavior of both histological subtypes of synovial sarcoma.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
1045-2257
|
pubmed:author |
pubmed-author:AkermanMM,
pubmed-author:Asko-SeljavaaraSS,
pubmed-author:BacchiniPP,
pubmed-author:ElomaaII,
pubmed-author:HuuhtanenRR,
pubmed-author:KnuutilaSS,
pubmed-author:LarssonOO,
pubmed-author:PiccoVV,
pubmed-author:SerraMM,
pubmed-author:SkyttingBB,
pubmed-author:SzymanskaJJ,
pubmed-author:TarkkanenMM,
pubmed-author:VirolainenMM
|
pubmed:issnType |
Print
|
pubmed:volume |
23
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
213-9
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:9790501-Adolescent,
pubmed-meshheading:9790501-Adult,
pubmed-meshheading:9790501-Aged,
pubmed-meshheading:9790501-Aged, 80 and over,
pubmed-meshheading:9790501-Aneuploidy,
pubmed-meshheading:9790501-Child,
pubmed-meshheading:9790501-Chromosome Deletion,
pubmed-meshheading:9790501-Female,
pubmed-meshheading:9790501-Gene Amplification,
pubmed-meshheading:9790501-Humans,
pubmed-meshheading:9790501-Male,
pubmed-meshheading:9790501-Middle Aged,
pubmed-meshheading:9790501-Nucleic Acid Hybridization,
pubmed-meshheading:9790501-Sarcoma, Synovial
|
pubmed:year |
1998
|
pubmed:articleTitle |
Genetic imbalances in 67 synovial sarcomas evaluated by comparative genomic hybridization.
|
pubmed:affiliation |
Department of Medical Genetics, Haartman Institute, University of Helsinki, Helsinki University Central Hospital, Finland.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|