**3.10. Pediatric diffuse astrocytic tumors**

Despite having a particular clinical evolution, pediatric tumors have been lumped together with the adult ones, according to the histopathological similarities [163]. We now know that their onset and progression genetic mechanisms are different. A well-defined entity that occurs predominantly in children is the one described above. As opposed to adult tumors,

**Figure 27.** T2W (a), FLAIR (b) and DWI (c) sequences of an infiltrative tumor into the brainstem and left cerebellar peduncles.

Diffuse Astrocytoma and Oligodendroglioma: An Integrated Diagnosis and Management http://dx.doi.org/10.5772/intechopen.76205 131

**Figure 28.** (a) T2W sequence of a diffuse infiltrative brainstem astrocytoma, partially resected; the 18 months follow-up MRI (b) demonstrates a stable lesion after radiotherapy.

the pediatric ones show changes in the genes regulating chromatin structure and the genetic expression profile. Apart from the diffuse midline glioma, H3 K27 M-mutant, another mutation present in the same gene, but in the G34 rather than the K27 position, defines another entity usually encountered in youths. The location differs, as it is no longer situated in the midline area, but in the brain hemispheres. High-grade astrocytic pediatric tumors with a telencephalic location show the TP53, CDK2A, ATRX, and SETD2 mutations [164]. The genetic syndromes that favor the onset of brain tumors during childhood are type 1 neurofibromatosis and Li-Fraumeni syndrome.
