The p73 gene encodes a protein structurally and functionally homologous to TP53, and maps to chromosomal band 1p36.33, where loss of heterozygosity has been observed in up to 90% of oligodendrogliomas and in 10-25% of diffuse astrocytomas.
The results of the p53 studies are consistent with findings of previous investigations that such mutations are less common in oligodendrogliomas than they are in astrocytomas.
In this study, we screened 28 oligodendrogliomas (WHO grade II) and 20 anaplastic oligodendrogliomas (WHO grade III) for alterations in the RB1/CDK4/p16INK4a/p15INK4b and TP53/p14ARF/MDM2 pathways.
Since accumulation of wild-type and mutant p53 are both associated with a poor prognosis, it is suggested to include immunohistochemical evaluation of p53 protein in routine diagnostics of oligodendrogliomas.
Using immunohistochemistry we evaluated the expression of two negative regulators of the cell cycle, the retinoblastoma gene product (pRb) and the WAF1/Cip1 gene product (p21), in consecutive paraffin sections from 54 gliomas (49 astrocytomas and 5 oligodendrogliomas) and related it to clinicopathological parameters, proliferative fraction, p53 expression and survival.
Considering the p53 labeling index and the apoptosis index together, this congenital oligodendroglioma may be regarded as potentially malignant despite the benign morphological features.
Histologically, those oligoastrocytomas with TP53 mutations were more often astrocytoma-predominant, while those with chromosome 19q loss were more often oligodendroglioma-predominant.
In conclusion, evaluation of p53 protein accumulation reflected the clinical course of oligodendrogliomas better than the mere presence of TP53 gene mutations.