Oligodendroglioma pathophysiology: Difference between revisions
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{{Oligodendroglioma}} | {{Oligodendroglioma}} | ||
==Overview== | ==Overview== | ||
==Pathophysiology== | |||
==Molecular genetics== | ===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.<ref>{{cite journal |author=Laigle-Donadey F, Benouaich-Amiel A, Hoang-Xuan K, Sanson M |title=[Molecular biology of oligodendroglial tumors] |language=French |journal=Neuro-Chirurgie |volume=51 |issue=3-4 Pt 2 |pages=260-8 |year=2005 |pmid=16292170 |doi=}}</ref><ref>{{cite journal |author=Walker C, Haylock B, Husband D, ''et al'' |title=Clinical use of genotype to predict chemosensitivity in oligodendroglial tumors |journal=Neurology |volume=66 |issue=11 |pages=1661-7 |year=2006 |pmid=16769937 |doi=10.1212/01.wnl.0000218270.12495.9a}}</ref> | 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.<ref>{{cite journal |author=Laigle-Donadey F, Benouaich-Amiel A, Hoang-Xuan K, Sanson M |title=[Molecular biology of oligodendroglial tumors] |language=French |journal=Neuro-Chirurgie |volume=51 |issue=3-4 Pt 2 |pages=260-8 |year=2005 |pmid=16292170 |doi=}}</ref><ref>{{cite journal |author=Walker C, Haylock B, Husband D, ''et al'' |title=Clinical use of genotype to predict chemosensitivity in oligodendroglial tumors |journal=Neurology |volume=66 |issue=11 |pages=1661-7 |year=2006 |pmid=16769937 |doi=10.1212/01.wnl.0000218270.12495.9a}}</ref> | ||
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. | 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. | ||
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==References== | ==References== | ||
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Revision as of 13:25, 10 September 2012
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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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.