PMID- 16167544
OWN - NLM
STAT- MEDLINE
DCOM- 20051027
LR  - 20181201
IS  - 0722-5091 (Print)
IS  - 0722-5091 (Linking)
VI  - 24
IP  - 5
DP  - 2005 Sep-Oct
TI  - Association of chromosome 7, chromosome 10 and EGFR gene amplification in 
      glioblastoma multiforme.
PG  - 209-18
AB  - Glioblastoma multiforme (GBM) is characterized by intratumoral heterogeneity in 
      both histomorphological and genetic changes, displaying a wide variety of 
      numerical chromosome aberrations, the most common of which are trisomy 7 and 
      monosomy 10. The amplification of the epidermal growth factor receptor (EGFR) 
      gene is the most frequently reported genetic abnormality. The associations 
      between these parameters and their implication in the tumoral progression are 
      poorly understood. We performed simultaneous fluorescence in situ hybridization 
      (FISH) with centromeric DNA probes for chromosomes 7 and 10 in smear 
      preparations, and EGFR gene amplification by PCR from 25 cases of GBM. Trisomy/ 
      polysomy for chromosome 7 was present in 76% of cases and monosomy 10 in 68%. 
      Both alterations were associated in 56% of cases. The EGFR gene was amplified in 
      52% of tumors; in 44% associated with trisomy/ polysomy 7, and in 36% with 
      monosomy 10. The three parameters were associated together in 28% of cases. 
      Kaplan-Meier survival rate analysis demonstrated lower survival rates in patients 
      with monosomy 10, trisomy 7, and monosomy associated with trisomy 7. The other 
      combinations were not different in frequency in relation to survival. In the 
      present study, trisomy/polysomy 7 and monosomy 10 have been found to be 
      frequently associated. The combination of both anomalies is probably important in 
      the tumorigenesis of glioblastoma. Moreover, this association is apparently 
      independent of EGFR gene amplification, which could be a later event in this 
      process.
FAU - Lopez-Gines, C
AU  - Lopez-Gines C
AD  - Department of Pathology, Medical School, University of Valencia, Spain. 
      concha.lopez@uv.es
FAU - Cerda-Nicolas, M
AU  - Cerda-Nicolas M
FAU - Gil-Benso, R
AU  - Gil-Benso R
FAU - Pellin, A
AU  - Pellin A
FAU - Lopez-Guerrero, J A
AU  - Lopez-Guerrero JA
FAU - Callaghan, R
AU  - Callaghan R
FAU - Benito, R
AU  - Benito R
FAU - Roldan, P
AU  - Roldan P
FAU - Piquer, J
AU  - Piquer J
FAU - Llacer, J
AU  - Llacer J
FAU - Barbera, J
AU  - Barbera J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Clin Neuropathol
JT  - Clinical neuropathology
JID - 8214420
RN  - 0 (Biomarkers, Tumor)
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Biomarkers, Tumor/analysis
MH  - Brain Neoplasms/*genetics/mortality/pathology
MH  - Child
MH  - Chromosomes, Human, Pair 10/*genetics
MH  - Chromosomes, Human, Pair 7/*genetics
MH  - ErbB Receptors/*biosynthesis/genetics
MH  - Female
MH  - *Gene Amplification
MH  - Glioblastoma/*genetics/mortality/pathology
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Middle Aged
MH  - Polymerase Chain Reaction
MH  - Prognosis
MH  - Survival Analysis
EDAT- 2005/09/20 09:00
MHDA- 2005/10/28 09:00
CRDT- 2005/09/20 09:00
PHST- 2005/09/20 09:00 [pubmed]
PHST- 2005/10/28 09:00 [medline]
PHST- 2005/09/20 09:00 [entrez]
PST - ppublish
SO  - Clin Neuropathol. 2005 Sep-Oct;24(5):209-18.