PMID- 25231439
OWN - NLM
STAT- MEDLINE
DCOM- 20150723
LR  - 20161214
IS  - 1098-2264 (Electronic)
IS  - 1045-2257 (Linking)
VI  - 54
IP  - 2
DP  - 2015 Feb
TI  - Array CGH analysis identifies two distinct subgroups of primary angiosarcoma of 
      bone.
PG  - 72-81
LID - 10.1002/gcc.22219 [doi]
AB  - Molecular genetic studies on vascular tumors are rare. Recently, possible 
      involvement of MYC and KDR has been documented in a subset of angiosarcomas of 
      soft tissue. We performed a cytogenetic analysis of primary angiosarcomas of bone 
      (n = 13) and soft tissue (n = 5) using high density array-comparative genomic 
      hybridization (array-CGH). Regions of interest were validated by fluorescence in 
      situ hybridization (FISH). Antibodies for candidate genes (SKI, MYC, KDR, and 
      MAPK9) were selected and immunohistochemistry was performed. Six angiosarcomas of 
      bone and four angiosarcomas of soft tissue showed chromosomal losses, gains, and 
      high level amplifications. Cluster analysis identified two groups: a group with a 
      complex genetic profile and a group with only few genetic aberrations. Five 
      regions of interest were selected, which were located at chromosome bands 
      1p36.23, 2q32-34, 5q35, 8q24, and 17q21.32-24.2. Interphase FISH confirmed the 
      high-level amplifications. Immunohistochemical analysis showed high expression of 
      MYC (16/60), MAPK9 (63/69), and SKI (52/62). There were no differences between 
      the two groups with regards to location, immunohistochemical expression nor 
      survival. In summary, we identified two subgroups of angiosarcoma: those with few 
      or no gross aberrations and those which show numerous genetic aberrations 
      consisting of chromosomal losses, gains and high level amplifications or complex 
      aberrations. The most common finding was amplification of 2q and 17q in both 
      angiosarcoma of bone and soft tissue, suggesting overlap in tumorigenesis 
      irrespective of their location. We show MYC amplification in primary angiosarcoma 
      indicating this is not entirely specific for radiation-induced angiosarcoma.
CI  - (c) 2014 Wiley Periodicals, Inc.
FAU - Verbeke, Sofie L J
AU  - Verbeke SL
AD  - Department of Pathology, University Medical Center Utrecht, Utrecht, The 
      Netherlands; Department of Pathology, Leiden University Medical Center, Leiden, 
      The Netherlands.
FAU - de Jong, Danielle
AU  - de Jong D
FAU - Bertoni, Franco
AU  - Bertoni F
FAU - Sciot, Raf
AU  - Sciot R
FAU - Antonescu, Cristina R
AU  - Antonescu CR
FAU - Szuhai, Karoly
AU  - Szuhai K
FAU - Bovee, Judith V M G
AU  - Bovee JV
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140918
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (MAP9 protein, human)
RN  - 0 (MYC protein, human)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 126648-96-2 (SKI protein, human)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Bone Neoplasms/*genetics
MH  - Chromosome Aberrations
MH  - Chromosomes, Human/*genetics
MH  - Comparative Genomic Hybridization
MH  - DNA-Binding Proteins/genetics
MH  - Female
MH  - Hemangiosarcoma/*genetics
MH  - Humans
MH  - Male
MH  - Microtubule-Associated Proteins/genetics
MH  - Middle Aged
MH  - Proto-Oncogene Proteins/genetics
MH  - Proto-Oncogene Proteins c-myc/genetics
EDAT- 2014/09/19 06:00
MHDA- 2015/07/24 06:00
CRDT- 2014/09/19 06:00
PHST- 2014/06/03 00:00 [received]
PHST- 2014/09/01 00:00 [accepted]
PHST- 2014/09/19 06:00 [entrez]
PHST- 2014/09/19 06:00 [pubmed]
PHST- 2015/07/24 06:00 [medline]
AID - 10.1002/gcc.22219 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2015 Feb;54(2):72-81. doi: 10.1002/gcc.22219. Epub 2014 
      Sep 18.