**4. Molecular genetics**

As in all gliomas, the origin of the tumor proceeds from the step-wise accumulation of genetic/ epigenetic alterations. Thirty-fifty percent of OAs exhibited loss of heterozygosity (LOH) on chromosomes 1p and 19q [20, 21], while approximately 30% of them harboured TP53 muta‐ tions. In particular, OAs of the temporal lobe more frequently exhibited TP53 mutations, and less commonly, 1p and 19q losses [22, 23].

OAII typically exhibited the type and distribution of genetic alterations observed in grade II gliomas [22]. OAIII showed genetic alterations commonly involved in the progression of astrocytic and oligodendroglial tumors, including loss of 9p with homozygous deletion of the cyclin-dependent kinase inhibitor 2A (CDKN2A) (p14ARF) gene, allelic loss on chromosome 10q and epidermal growth factor receptor (EGFR) gene amplification [24].
