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- Title
Tumour necrosis and microvascular proliferation are associated with 9p deletion and CDKN2A alterations in 1p/19q -deleted oligodendrogliomas.
- Authors
Godfraind, C.; Rousseau, E.; Ruchoux, M.-M.; Scaravilli, F.; Vikkulat, M.
- Abstract
A subset of oligodendrogliomas and oligoastrocytomas has been associated with 1p /19q deletion. Subsequently, this genetic alteration was linked to chemosensitivity and classic histology of oligodendrogliomas. Tumoural progression includes deletions of 9p , 10q and alterations of CDKN2A . However, these (epi)genetic changes have not been associated with specific histological features. In a series of 45 gliomas including oligodendrogliomas, oligoastrocytomas and astrocytomas, deletions of chromosomal regions implied in these tumours (1p , 9p , 10 , 17p13 , 19q and 22 ) were looked for by microsatellite analysis. Tumours that were deleted for 1p and 19q were selected. Subsequently, presence of deletions in the other studied regions, (epi)genetic changes in p14 [sup ARF ] , CDKN2A and CDKN2B , as well as histological features, were associated to these tumours. 1p/19q deletion was observed in 22 tumours. Twenty-one of them presented regions of classic histology of oligodendroglioma. A deletion of 9p was found in eight of them, always in association with tumour necrosis and/or microvascular proliferation. In addition, (epi)genetic alterations of CDKN2A were observed in 71% of these tumours. Presence of regions of classic histology of oligodendroglioma in a tumour sample is predictive of 1p/19q deletions. Necrosis and/or microvascular proliferation are signs of an additional 9p deletion. Finally, as CDKN2A (epi)genetic alterations were found in 71% of the 1p/19q/9p -deleted oligodendrogliomas, CDKN2A may have a role in oligodendroglioma-associated microvascular proliferation.
- Subjects
ASTROCYTOMAS; OLIGODENDROGLIA; MICROSATELLITE repeats; TUMOR necrosis factors
- Publication
Neuropathology & Applied Neurobiology, 2003, Vol 29, Issue 5, p462
- ISSN
0305-1846
- Publication type
Article
- DOI
10.1046/j.1365-2990.2003.00484.x