**2.1. Incidence**

**1. Introduction**

340 Neurooncology - Newer Developments

remained unsolved [9].

In the 2007 World Health Organization (WHO) classification of the central nervous system (CNS) tumors [1], oligoastrocytoma (OA) was considered as a mixed glioma with an astro‐ cytic and an oligodendroglial component [2, 3]. It could be easily recognized if the two components were clearly separated, as it rarely happened. Usually, the two cell types were found intermingled and the differential diagnosis towards astrocytomas and oligodendro‐ gliomas was difficult and, frequently, it remained undefined. Since its first recognition [4] and confirmation [5], its definability was poor and the tumor was even considered as an oligoden‐ droglioma with reactive astrocytes [6]. The poor tumor definability explains why the preva‐ lence of OAs in the various collections of the literature has been so variable and it accounted for the need to establish criteria useful for the recognition of the tumor. It was suggested to rely on the occurrence of at least 10% neoplastic oligodendrocytes in astrocytic gliomas [7] or 10% neoplastic astrocytes in oligodendroglial gliomas [8], provided that oligodendrocytes were neoplastic and not normal, and that astrocytes were tumor and not reactive. These criteria, however, were too vague in the clinical practice and the definition of the tumor remained a subjective matter. In particular, the recognition of normal from tumor oligoden‐ drocytes, especially in slightly infiltrating or diffuse growth where the cell density is low,

As a matter of fact, the diagnostic uncertainties of OA were also due to the lack of a reliable marker for tumor oligodendrocytes in tissue sections. The prevailing diffuse and infiltrating growth of both oligodendrogliomas and the oligodendroglial component of OAs led to find the coexistence in the same tumor area of tumor and normal oligodendrocytes to the point that it was even difficult to establish, in some cases, whether a tumor infiltration existed or not. On the other hand, the difficulty to recognize a mild oligodendroglial infiltration in oligodendro‐ gliomas themselves was already known, even exploiting the occurrence of abnormal nuclei or

Another critical point was the difficulty to distinguish reactive from tumor astrocytes and to recognize the real nature of minigemistocytes [10], glial fibrillary oligodendrocytes (GFOC)

The origin of the tumor was referred to a progenitor stage preceding the astrocytic and oli‐ godendroglial differentiation and, therefore, tumor suppressor protein p53 (TP53) mutations were searched for in the astrocytic component and the 1p/19q co-deletion in the oligoden‐ droglial one and a genetic analysis was suggested [14]. Anyway, the variability of OA prev‐ alence in the various collections remained high. It was observed that the absence of 1p/19q co-deletion, typical of oligodendrogliomas, entailed the occurrence of TP53 mutations [15], but also that it could be present or absent in both tumor components and that all tumor cells

crowding of tumor cells along capillaries or around neurons.

[11–13], real gemistocytes, and perineural satellites.

seemed to share the same genetic aberrations [14].

OA was the third most common glioma. It accounted for 1% of all brain tumors and 5–10% of all glial neoplasms. The incidence of OA was approximately 0.03 *per* 100,000 individuals in the United States. Young and middle-aged adult population was affected. The median age of diagnosis was 42 years. Males were more commonly affected than females; the male to female ratio was approximately 1.43–1. OA usually affected individuals of the Caucasian race with a higher incidence rate in developed countries [1].
