Adult gliomas are most often infiltrative. The World Health Organization (WHO) 
has classed them into three major groups according to the presomptive cell of 
origin: astrocytoma, oligodendroglioma and mixed oligoastrocytoma. Depending on 
the presence or absence of a small number of signs of anaplasia (mitosis, 
nuclear atypia, cell density, microvascular proliferation and necrosis) the WHO 
distinguishes grade II (LGG), III (anaplastic), and IV (glioblastomas, GBM). 
Mutation in the isocitrate deshydrogenase I and II (IDH1 and 2) genes 
distinguishes grade II, III and secondary GBM from primary GBM. Moreover two 
additional genetic alterations are recorded in grade II and III gliomas: TP53 
mutations that characterize astrocytomas and 1p19q codeletion (as the result of 
t(1;19)(q10;p10) translocation) recorded in oligodendrogliomas. Mixed gliomas, 
the most non-reproducible category, share with astrocytomas and 
oligodendrogliomas the same genetic alterations. Interestingly TP53 mutation 
(p53+) and 1p19q codeletion (1p19q+) are mutually exclusive and involve IDH 
mutated (IDH+) glial precursor cells. According to IDH, TP53, and 1p19q status, 
four major subtypes of LGG are recorded: IDH+/p53-/1p19q-, IDH+/p53+/1p19q-, 
IDH+/p53-/1p19q+ and triple negative, this last subgroup having the worst 
prognosis. Interestingly, p53 expression and internexin alpha (INA) expression 
can replace to some extent TP53 mutation and 1p19 codeletion, respectively. 
Moreover the antibody directed against the IDH1R132H isoform is highly specific. 
Because this mutation is the most frequent it is sufficient to assess IDH status 
in more than 80% of grade II and III gliomas. Taken together these three 
immunohistochemical markers are contribute greatly to the classification of 
gliomas and should be tested routinely as diagnostic markers. Finally, although 
GBM are genetically heterogeneous, the vast majority display EGFR amplification, 
often associated with EGFR expression, which can be helpful for diagnosis in 
certain cases.