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The term “oligodendroglioma” was coined by Bailey et al. [1, 19] according to the resemblance of these lesions to normal oligodendrocytes. The “classic” histology of these neoplasms includes round cell nuclei of a constant size surrounded by a ring of very feebly stained cytoplasm, a network of fine capillaries, and calcifications [2–4]. As formalin fixation makes the cytoplasm of the neoplastic cells swollen, their membrane becomes well-defined, exhibiting a honeycomb or “fried egg” appearance [2, 3]. Currently there is no uniformly accepted histopathological grading scheme of oligodendroglial tumors and differentiation of OD (WHO grade II) and anaplastic OD (AOD; WHO grade III) is rather controversial [4].

The tumor abundantly expresses Nkx-2.2 homeodomain protein, as well as the oligodendrocyte lineage-specific basic helix-loop-helix OLIG family of transcription factors, in particular OLIG2 [20]. The latter is widely present in embryonic brain, where it interacts with Nkx-2.2 directing ventral neuronal patterning in response to graded Sonic Hedgehog (SHH) signaling in the embryonic neural tube [21]. Nonetheless, to date no convincing evidence (e.g., expression of the myelin-related proteins or identification of myelin formation on electron microscopy) supports an oligodendroglial origin of OD, thus it is considered that these tumors arise from unknown progenitor cells of the embryonic neural tube.

Lack of specific IHC markers has resulted previously in considerable interobserver disagreement regarding the diagnosis of OD/AOD. However, the updated WHO classification of CNS tumors (2016) [11] based on molecular profile has resolved this problem. It presumes that the term “oligodendroglioma” should be applied only for neoplasms with IDH1/IDH2 mutation and 1p/19q co-deletion (unless the lesion is NOS) [11]. Previous genetic studies repeatedly demonstrated that 1p/19q co-deletion is almost mutually exclusive with TP53 mutation in gliomas, and that “classic” morphology of OD is strongly associated with this cytogenetic abnormality. Of note, now there is a general agreement that to support diagnosis of OD/AOD 1p/19q co-deletion needs to encompass the entire arms of both chromosomes, since partial losses have been observed frequently in other types of gliomas [12].