It looks like there have been some changes in the diagnosis of gliomas. I copied the following from the link that Flipper gave.
Box 1 Key new developments in the diagnosis and management of gliomas (2016–2020)
Glioblastoma is now defined as a diffuse astrocytic glioma with no mutations in IDH genes nor histone H3 genes and is characterized by microvascular proliferation, necrosis and/or specific molecular features, including TERT promoter mutation, EGFR gene amplification and/or a +7/–10 cytogenetic signature.
IDH-mutant glioblastoma is now referred to as IDH-mutant astrocytoma, WHO grade 4.
Homozygous deletion of CDKN2A/B locus is a molecular marker of WHO grade 4 in IDH-mutant astrocytomas.
Histone H3.3 G34-mutant diffuse hemispheric gliomas constitute a novel glioma entity corresponding to WHO grade 4.
The value of the distinction between WHO grades 2 and 3 in IDH-mutant gliomas is increasingly challenged, and ongoing clinical trials (such as CODEL[83] and EORTC 1635 (ref.125)) are enrolling patients with tumours of both grades.
In the CATNON trial[89], the combination of maintenance temozolomide with radiotherapy prolonged survival only in patients with IDH-mutant gliomas of WHO grade 3 and not in those with tumours diagnosed as IDH-wild-type anaplastic gliomas.
The prolongation of maintenance temozolomide from 6 to 12 cycles extends neither progression-free survival nor overall survival[106].
Bevacizumab does not prolong progression-free survival nor overall survival in patients with 1p/19q-intact recurrent WHO grade 2 or 3 glioma14.
Nivolumab is not superior to bevacizumab in patients with recurrent glioblastoma[119].
Nivolumab is not superior to temozolomide in patients with newly diagnosed glioblastoma without MGMT promoter methylation100.