**6. New criteria for glioma diagnosis after the "ISN-Haarlem Consensus"**

Our knowledge on the nature of OA underwent a profound change after the "International Society of Neuropathology (ISN)-Haarlem *Consensus*" guidelines led to the official recogni‐ tion of the indispensability of the genetic analysis in order to obtain an "integrated" diagno‐ sis of gliomas [28]. Referred to grade II and III adult gliomas, this new approach would involve a combination of histologic and molecular data based on the 1p/19q, isocitrate dehydrogen‐ ase (IDH) 1/2 and α-thalassemia/mental retardation syndrome X-linked (ATRX) status.

#### **6.1. 1p/19q chromosomal status**

The genetic hallmark of oligodendroglial tumors is a combined chromosomal deletion of the short arm of the chromosome 1 (1p) and the long arm of the chromosome 19 (19q). Com‐ bined 1p and 19q losses were described in 80–90% of grade II and in 50–70% of grade III tumors [22, 24].

The 1p/19q chromosomal status was recognized as an important diagnostic biomarker in the clinical practice. The 1p/19q co-deletion was reported in 60–70% of oligodendrogliomas with a classical histologic phenotype (perinuclear "halo" and "chicken wire" vascular pattern). Partial 1p or 19q deletion occurred in approximately 75% of the cases [29, 30]. Oligodendro‐ glial tumors with 1p/19q co-deletion were observed to typically arise at an extra-temporal location, whereas tumors with intact 1p/19q at the temporal lobe [22]. In contrast, childhood oligodendrogliomas only rarely exhibited chromosomal abnormalities.

Importantly, the occurrence of 1p/19q co-deletion supports the diagnosis of oligodendroglio‐ ma, especially when histology is atypical. However, its absence does not exclude this diagno‐ sis, leaving unsolved the question of oligodendrogliomas with intact 1p/19q.

In OA, the frequency of the 1p/19q co-deletion was approximately 50% [22]. Virtually, it was mutually exclusive with LOH of chromosome 17p13 and TP53 mutations, both typical of astrocytic tumors. In OA, the 1p/19q co-deletion was referred to the oligodendroglial compo‐ nent, whereas TP53 mutations to the astrocytic one.
