Combining two biomarkers, IDH1/2 mutations and 1p/19q codeletion, to stratify anaplastic oligodendroglioma in three groups: a single-center experience.
We found 165 IDH1 (72.7%) and 2 IDH2 mutations (0.9%) in 227 diffuse astrocytomas WHO grade II, 146 IDH1 (64.0%) and 2 IDH2 mutations (0.9%) in 228 anaplastic astrocytomas WHO grade III, 105 IDH1 (82.0%) and 6 IDH2 mutations (4.7%) in 128 oligodendrogliomas WHO grade II, 121 IDH1 (69.5%) and 9 IDH2 mutations (5.2%) in 174 anaplastic oligodendrogliomas WHO grade III, 62 IDH1 (81.6%) and 1 IDH2 mutations (1.3%) in 76 oligoastrocytomas WHO grade II and 117 IDH1 (66.1%) and 11 IDH2 mutations (6.2%) in 177 anaplastic oligoastrocytomas WHO grade III.
A total of 221 somatic IDH1 mutations were detected and the highest frequencies occurred in diffuse astrocytomas (68%), oligodendrogliomas (69%), oligoastrocytomas (78%) and secondary glioblastomas (88%).
In the current study, we found that overexpression of OLIG2 was not only found in oligodendroglioma samples and normal neural tissue but also in a wide spectrum of malignant cell lines including leukemia, non-small cell lung carcinoma, melanoma, and breast cancer cell lines.
The markers p53 and MIB-1 were significantly higher expressed in astrocytomas than in oligodendrogliomas and expression levels of p53 and EGFR were inversely associated within the astrocytic group.
The markers p53 and MIB-1 were significantly higher expressed in astrocytomas than in oligodendrogliomas and expression levels of p53 and EGFR were inversely associated within the astrocytic group.
High OLIG expression alone has been proposed to distinguish oligodendrogliomas from astrocytomas, so we critically evaluated OLIG2 as a marker by immunohistochemical and oligonucleotide microarray analysis.
Herein, we report on comparative genomic hybridization (CGH) and immunohistochemical (IHC) assessment of EGFR, PTEN, p53, and MIB-1 expression in 13 oligodendrogliomas (10 WHO grade II, 3 WHO grade III), one oligoastrocytoma (WHO grade III) and 23 high-grade astrocytomas (3 WHO grade III, 20 glioblastoma multiforme).
The markers p53 and MIB-1 were significantly higher expressed in astrocytomas than in oligodendrogliomas and expression levels of p53 and EGFR were inversely associated within the astrocytic group.
Cases with oligodendrogliomas with the 19q deletion had a significantly higher frequency of the GLTSCR1-exon-1 T allele compared with cases without the 19q deletion (P = 0.01).
Recent studies of 1p/19q co-deleted OD suggest that the NOTCH2 gene is implicated in oligodendrocyte differentiation and may be involved in this rearrangement.
In patients affected by WHO grade II oligodendroglioma, median survival was 24 and 96 months, respectively, in COX-2 positive and negative lesions (P =0.012).
Whereas a mutation was not detected in the coding region of the SHREW1 gene in oligodendrogliomas, restoration of SHREW1 expression resulted in suppression of cell adhesion and migration.
Abnormal expression of peroxiredoxin 6 and rho GDP dissociation inhibitor alpha may be associated with malignant transformation in oligodendroglioma and these proteins might be candidates of molecular predictive factors.