It has become increasingly evident that morphologically similar gliomas may have 
distinct clinical phenotypes arising from diverse genetic signatures. To date, 
glial tumours from the Tunisian population have not been investigated. To 
address this, we correlated the clinico-pathology with molecular data of 110 
gliomas by a combination of HM450K array, MLPA and TMA-IHC. PTEN loss and EGFR 
amplification were distributed in different glioma histological groups. However, 
1p19q co-deletion and KIAA1549:BRAF fusion were, respectively, restricted to 
Oligodendroglioma and Pilocytic Astrocytoma. CDKN2A loss and EGFR overexpression 
were more common within high-grade gliomas. Furthermore, survival statistical 
correlations led us to identify Glioblastoma (GB) prognosis subtypes. In fact, 
significant lower overall survival (OS) was detected within GB that 
overexpressed EGFR and Cox2. In addition, IDH1R132H mutation seemed to provide a 
markedly survival advantage. Interestingly, the association of IDHR132H mutation 
and EGFR normal status, as well as the association of differentiation markers, 
defined GB subtypes with good prognosis. By contrast, poor survival GB subtypes 
were defined by the combination of PTEN loss with PDGFRa expression and/or EGFR 
amplification. Additionally, GB presenting p53-negative staining associated with 
CDKN2A loss or p21 positivity represented a subtype with short survival. Thus, 
distinct molecular subtypes with individualised prognosis were identified. 
Interestingly, we found a unique histone mutation in a poor survival young adult 
GB case. This tumour exceptionally associated the H3F3A G34R mutation and MYCN 
amplification as well as 1p36 loss and 10q loss. Furthermore, by exhibiting a 
remarkable methylation profile, it emphasised the oncogenic power of G34R 
mutation connecting gliomagenesis and chromatin regulation.