Oligodendroglioma pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Oligodendroglioma Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Oligodendroglioma pathophysiology On the Web |
American Roentgen Ray Society Images of Oligodendroglioma pathophysiology |
Risk calculators and risk factors for Oligodendroglioma pathophysiology |
Overview
Pathophysiology
Molecular genetics
By far, the most common structural deformity found is co-deletion of chromosomal arms 1p and 19q. The high frequency of co-deletion (60-80%) is a striking feature of this glial tumour, and is considered as a "genetic signature" of oligodendroglioma. 1p/19q deletion has been correlated with both chemosensitivity and improved prognosis in oligodendrogliomas.[1][2] A t(1;19)(q10;p10) translocation mediates the combined deletions of 1p and 19q. The gene products lost as a consequence of this codeletion may include mediators of resistance to genotoxic therapies. Alternatively, 1p/19q loss might be an early oncogenic lesion promoting the formation of glial neoplasms, which retain high sensitivity to genotoxic stress.
References
- ↑ Laigle-Donadey F, Benouaich-Amiel A, Hoang-Xuan K, Sanson M (2005). "[Molecular biology of oligodendroglial tumors]". Neuro-Chirurgie (in French). 51 (3-4 Pt 2): 260–8. PMID 16292170.
- ↑ Walker C, Haylock B, Husband D; et al. (2006). "Clinical use of genotype to predict chemosensitivity in oligodendroglial tumors". Neurology. 66 (11): 1661–7. doi:10.1212/01.wnl.0000218270.12495.9a. PMID 16769937.