PMID- 18095137
OWN - NLM
STAT- MEDLINE
DCOM- 20081014
LR  - 20181201
IS  - 1433-7398 (Print)
IS  - 1433-7398 (Linking)
VI  - 24
IP  - 1
DP  - 2007
TI  - FISH 1p/19q deletion/imbalance for molecular subclassification of glioblastoma.
PG  - 1-5
AB  - Glioblastoma is the most malignant and frequent of the glial tumors. A minor 
      fraction of glioblastoma may contain areas showing oligodendroglioma-like tumor 
      cell differentiation. Several authors have described such tumors as glioblastoma 
      with oligodendroglial component (GBMO). GBMO may represent the ultimate level of 
      malignancy in the oligodendroglial lineage. The oligodendroglial component and 
      combined loss of chromosomal arm 1p and 19q in glioblastoma indicate increased 
      survival. In our study, we analyzed 1p and 19q status in a series of 12 
      glioblastoma and 8 oligodendroglial tumors using fluorescence in situ 
      hybridization (FISH) on paraffin-embedded tissues. In each case, hybridization 
      status was classified as deletion, imbalance, polysomy, amplification, or normal 
      pattern. Other genetic alterations such as CDKN2A (p16), RB, and EGFR were also 
      assessed. On histological review, 2 of 12 glioblastoma (16.7%) were classified as 
      GBMO. Chromosome 1p/19q deletion was detected in 3 of 12 glioblastomas (25%). In 
      contrast, all 8 oligodendroglial tumors showed 1p/19q deletion. All GBMO had 19q 
      deletion with imbalance, whereas 1 of 10 ordinary glioblastoma (10%) demonstrated 
      19q deletion with imbalance. All but 1 ordinary glioblastoma (90%) showed CDKN2A 
      (p16) deletion, but no GBMO displayed this alteration. Our results indicate that 
      GBMO may be a distinct subtype of glioblastoma harboring a characteristic 
      molecular profile. FISH on paraffin-embedded specimens is a useful method for 
      subclassification of glioblastoma.
FAU - Nagasaka, Toru
AU  - Nagasaka T
AD  - Department of Neurosurgery, Japanese Red Cross Nagoya First Hospital, Nagoya, 
      453-8511, Japan. toru-ngy@umin.ac.jp
FAU - Gunji, Masaharu
AU  - Gunji M
FAU - Hosokai, Noboru
AU  - Hosokai N
FAU - Hayashi, Kumiko
AU  - Hayashi K
FAU - Ikeda, Hiroshi
AU  - Ikeda H
FAU - Ito, Masafumi
AU  - Ito M
FAU - Inao, Suguru
AU  - Inao S
LA  - eng
PT  - Journal Article
DEP - 20070525
PL  - Japan
TA  - Brain Tumor Pathol
JT  - Brain tumor pathology
JID - 9716507
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Brain Neoplasms/classification/*genetics
MH  - Chromosome Deletion
MH  - ErbB Receptors/genetics
MH  - Gene Amplification
MH  - Glioblastoma/classification/*genetics
MH  - Humans
MH  - *In Situ Hybridization, Fluorescence
EDAT- 2007/12/21 09:00
MHDA- 2008/10/15 09:00
CRDT- 2007/12/21 09:00
PHST- 2006/07/10 00:00 [received]
PHST- 2006/08/25 00:00 [accepted]
PHST- 2007/12/21 09:00 [pubmed]
PHST- 2008/10/15 09:00 [medline]
PHST- 2007/12/21 09:00 [entrez]
AID - 10.1007/s10014-006-0209-6 [doi]
PST - ppublish
SO  - Brain Tumor Pathol. 2007;24(1):1-5. doi: 10.1007/s10014-006-0209-6. Epub 2007 May 
      25.