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glioblastoma

Saturday 6 November 2004

Loss of heterozygosity (Allelotyping) (#12875726#)

3q25.2-26.2 LOH
4q31.1-31.2 LOH
4q35 LOH
6q21-23.3 LOH
6q27 LOH
9p21-23 LOH 31% CDKN2A (p16) CDKN2B (p15)
9q LOH
10p12.2-14 LOH
10q LOH 69%
10q21.3 LOH
10q23 LOH 24%-69% PTEN
10q25.3-q26.1 LOH DMBT1
11p12-13 LOH
13q12.1-14.1 LOH
13q14.3-31 LOH RB
14q11.1-13 LOH
14q13-31 LOH
14q32.1 LOH
Chr.15 LOH
17p11.2-12 LOH
17p13 LOH 31% TP53
19q LOH
22q13.3 LOH

Gene inactivations

TP53 31% 17p13
CDKN2A (p16) 31% 9p21
PTEN 24% 10q23

- Glioblastomas frequently carry mutations in the PTEN tumor suppressor gene on 10q23.3 (24%).

Gene overexpressions

- EGFR amplification (34%)

Amplified regions and gene copy increases (chromosome gains, genic amplifications)

- Chr.7 (radiation resistance) (#16130123#)
- Chr.1
- Chr.4
- Chr.11
- Chr.12

Molecular pathways

- genetic alterations and aberrant expression of genes related to the phosphatidyl-inositol-3’-kinase/protein kinase B (Akt) signal transduction pathway in glioblastoma (#14655756#)

Variants

- primary glioblastoma (de novo) prevailed (95%)
- secondary glioblastoma

References

- Ohgaki H. Genetic pathways to glioblastomas. Neuropathology. 2005 Mar;25(1):1-7. PMID: #15822813#

References

- Gilbertson RJ, Rich JN. Making a tumour’s bed: glioblastoma stem cells and the vascular niche. Nat Rev Cancer. 2007 Oct;7(10):733-6. PMID: #17882276#

- Knobbe CB, Reifenberger G. Genetic alterations and aberrant expression of genes related to the phosphatidyl-inositol-3’-kinase/protein kinase B (Akt) signal transduction pathway in glioblastomas. Brain Pathol. 2003 Oct;13(4):507-18. PMID: #14655756#