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There is accumulating evidence that tumors of the same histological group and similar genetic abnormalities exhibit uniform responses to management and carry comparable prognosis. Moreover, the molecular characteristics of the lesion may be helpful for choosing an optimal individualized treatment strategy, particularly with regard to adjuvant therapy [7, 14, 17, 51, 78]. Additionally, the genetic fingerprint of pathological tissue may be very helpful for establishment of the correct diagnosis from small volume biopsy samples [6]. Thus it seems rational that genetic characteristics of gliomas were incorporated into the updated WHO classification of CNS tumors (2016) [11]. While in some pathological entities histology alone may remain the basis for diagnostic definitions, for others molecular data should be used for lesion characterization with the clear distinction of “molecularly defined” and “non-molecularly defined” groups [10, 11].

Table 3. Framework for possible histopathological classification of WHO grade II gliomas in adults (according to the ISN-Haarlem consensus guidelines [10])

It can be expected, however, that with this approach some gliomas may not fit into predefined categories [11]. For instance, neoplasms with mixed or ambiguous morphology and/or non-typical genetic abnormalities may favor a pathological definition of “diffuse glioma” with designation of the molecular alterations or without further specification (Table 3) [4, 10, 11]. On the other hand, IDH wild-type AA with combined +7p/–10q or +7q/–10q may be probably classified as GBM [9, 12]. In some rare situations there might be unusual combinations of histological and molecular data that necessitate descriptive diagnosis, but even in such pathologically ambiguous cases profiling major genetic and/or cytogenetic abnormalities may help clinicians to determine appropriate treatment and define prognosis [4, 10].