
GENETIC STUDIES OF C-MIC ONCONGENE AND RORI GENE OVEREXPRESSION IN EPENDYMOMAS YUEMIN DING Neuro-oncology Group Department of Molecular Neuroscience Institute of Neurology Queen Square,London Supervisor:Dr Tracy Warr
GENETIC STUDIES OF C-MYC ONCONGENE AND ROR1 GENE OVEREXPRESSION IN EPENDYMOMAS YUEMIN DING Neuro-oncology Group Department of Molecular Neuroscience Institute of Neurology Queen Square, London Supervisor: Dr Tracy Warr

Institute of Neurology (Queen Square) UCL University College London

BACKGROUND Ependymomas are glial tumors that arise from the ependymal lining of the ventricular system of the CNS. They represent the third most frequent brain tumor in children. (Hamilton RL et al.1997) The genetic events that contribute to the pathogenesis of paediatric ependymoma are poorly defined. (Ward S et al.2001)
BACKGROUND • Ependymomas are glial tumors that arise from the ependymal lining of the ventricular system of the CNS. • They represent the third most frequent brain tumor in children. (Hamilton RL et al. 1997) • The genetic events that contribute to the pathogenesis of paediatric ependymoma are poorly defined. (Ward S et al. 2001)

BACKGROUND Previous finding of our group The expression of >12,000 genes in a set of 11 ependymoma samples were determined using oligonucleotide micrarrays analysis.Oncogene c-myc and gene RORI were identified to be highly expressed in the tumour samples. Previous experiments failed to show extra copies of c- myc gene in ependymomas by comparative genomic hybridization (CGH)and fluorescence in situ hybridization (FISH)
BACKGROUND • The expression of >12,000 genes in a set of 11 ependymoma samples were determined using oligonucleotide micrarrays analysis. Oncogene c-myc and gene ROR1 were identified to be highly expressed in the tumour samples. • Previous experiments failed to show extra copies of cmyc gene in ependymomas by comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH). Previous finding of our group

BACKGROUND c-nyc oncogene CHR #8 ⅫD 程黄:月销月:自期销目::目目弱8 c-Myc 5 ↓! 9439 Cellular Cell growth processes apoptosis proliferation differentiation
BACKGROUND c-myc oncogene c-Myc CHR # 8 Cell growth proliferation differentiation apoptosis Cellular processes

BACKGROUND CANCER c-Myc c-Myc c-Myc c-Myc Mye c-Myc 著。ye -Me e-Mye -c-myc has emerged as a central oncogenic switch in many human cancers.(Stella Pelengaris 2002)
BACKGROUND c-Myc c-Myc c-Myc c-Myc c-Myc c-Myc c -Myc c -Myc c -Myc c -Myc ! — c-myc has emerged as a central oncogenic switch in many human cancers. (Stella Pelengaris 2002)

BACKGROUND Mechanisms lead to gene overexpression Chromosome duplication ·Gene amplification 。Point mutation .Regulators dysfunction
BACKGROUND Mechanismslead to gene overexpression • Chromosome duplication • Gene amplification • Point mutation • Regulators dysfunction

overexpression of normal product chromosome gene point mutation duplication amplification A-T A-T G G G G-C G-C A-T T-A T-A
overexpression of normal product chromosome duplication gene amplification point mutation A - T C - G G - C A - T T - A A - T C - G G - C G - C T - A

overexpression of normal product activator operator regulator promoter structural gene mRNA mRNA repressor active protein protein Loss of function mutation
overexpression of normal product Loss of function mutation

BACKGROUND Previous finding of our group .The expression of >12,000 genes in a set of 11 ependymoma samples were determined using oligonucleotide micrarrays analysis.Oncogene c-myc and gene RORI were identified to be highly expressed in the tumour samples. Previous experiments failed to show extra copies of c- myc gene in ependymomas by comparative genomic hybridization (CGH)and fluorescence in situ hybridization(FISH)
BACKGROUND • The expression of >12,000 genes in a set of 11 ependymoma samples were determined using oligonucleotide micrarrays analysis. Oncogene c-myc and gene ROR1 were identified to be highly expressed in the tumour samples. • Previous experiments failed to show extra copies of cmyc gene in ependymomas by comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH). Previous finding of our group