PMID- 16102584
OWN - NLM
STAT- MEDLINE
DCOM- 20051006
LR  - 20191210
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 161
IP  - 2
DP  - 2005 Sep
TI  - Identification of oligodendroglioma specific chromosomal copy number changes in 
      the glioblastoma MI-4 cell line by array-CGH and FISH analyses.
PG  - 140-5
AB  - Glioblastomas, the most frequent and malignant glial tumors, are known to be 
      phenotypically heterogeneous. A low fraction of glioblastomas is associated with 
      specific chromosomal losses at 1p and 19q, which are commonly found in 
      oligodendrogliomas and are generally considered to be a primary event in the 
      development of these tumors. Subsequent progression of oligodendroglial tumors 
      appears to be triggered by additional molecular features underlying the 
      transition to anaplastic oligodendroglioma and glioblastoma multiforme (GBM) such 
      as deletions of 9p and 10q, and alterations of CDKN2A (p16), which is located at 
      9p21. These findings strengthen the view that GBM on rare occasions may develop 
      from oligodendroglial differentiated cells. In the present study, we evaluated 
      the newly established MI-4 glioblastoma cell line, which displays 1p and 19q 
      specific alterations targeting preferential regions of allelic loss in glial 
      neoplasms, by array-CGH and fluorescence in situ hybridization (FISH) analyses 
      that were combined to obtain a high resolution map of targeted chromosome 
      rearrangements and copy number changes throughout the genome. Genome-wide and 
      chromosome 19 full coverage array-CGH analysis of the MI-4 cell line revealed 
      that in this particular cell line, 1p-specific loss, including the CDKN2 (p18) 
      gene, is not accompanied by loss of the previously described 19q13.3 tumor 
      suppressor candidate region. Interestingly, the array-CGH (CGHa) profile showed 
      an increase in copy number along most of 19q including the AKT2 oncogene and the 
      KLKs gene family, which have previously been shown to be amplified in pancreatic 
      carcinomas and upregulated in several tumors, respectively. The concomitant 1p 
      partial loss and chromosome 19 alterations, with the +7 and -10-specific GBM 
      markers associated with homozygous deletion of 9p21.3 including CDKN2A (p16), are 
      distinct features of the glioblastoma MI-4 cell line, illustrating its origin 
      from an olidodendroglial tumor. Based on these results, we conclude that the MI-4 
      glioblastoma cell line might function as a model system for investigations into 
      the behavior of a defined oligodendroglioma subtype.
FAU - Magnani, Ivana
AU  - Magnani I
AD  - Department of Biology and Genetics, University of Milan, via Viotti3/5, 20133 
      Milan, Italy.
FAU - Moroni, Ramona Frida
AU  - Moroni RF
FAU - Roversi, Gaia
AU  - Roversi G
FAU - Beghini, Alessandro
AU  - Beghini A
FAU - Pfundt, Rolph
AU  - Pfundt R
FAU - Schoenmakers, Eric F
AU  - Schoenmakers EF
FAU - Larizza, Lidia
AU  - Larizza L
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
SB  - IM
EIN - Cancer Genet Cytogenet. 2005 Nov;163(1):99. Ramona, Ramona Frida [corrected to 
      Moroni, Ramona Frida]
MH  - Brain Neoplasms/*genetics
MH  - *Cell Line, Tumor
MH  - *Chromosome Aberrations
MH  - *Chromosomes, Human, Pair 1
MH  - Chromosomes, Human, Pair 19
MH  - Gene Dosage
MH  - Glioblastoma/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Microarray Analysis
MH  - Oligodendroglioma/*genetics
EDAT- 2005/08/17 09:00
MHDA- 2005/10/07 09:00
CRDT- 2005/08/17 09:00
PHST- 2004/11/17 00:00 [received]
PHST- 2005/02/02 00:00 [revised]
PHST- 2005/02/08 00:00 [accepted]
PHST- 2005/08/17 09:00 [pubmed]
PHST- 2005/10/07 09:00 [medline]
PHST- 2005/08/17 09:00 [entrez]
AID - S0165-4608(05)00110-X [pii]
AID - 10.1016/j.cancergencyto.2005.02.010 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2005 Sep;161(2):140-5. doi: 
      10.1016/j.cancergencyto.2005.02.010.