Figure 1.
Gliomas of frontal, temporal and insular origin had significantly different pathological constituents of tumor subsets.
The percentage of astrocytoma in gliomas of the frontal origin (15.1%) was significantly lower than that of non-frontal origin (24.2%) (P = 0.011). The percentage of glioblastoma in gliomas of the frontal origin (12.8%) was significantly lower than that of non-frontal origin (19.4%) (P = 0.048). The percentage of oligodendroglioma in gliomas of the frontal origin (18.8%) was significantly higher than that of non-frontal origin (12.6%) (P = 0.049). The percentage of glioblastoma in gliomas of the temporal origin (31.3%) was significantly higher than that of non-temporal origin (12.6%) (P<0.001). The percentage of oligodendroglioma in gliomas of the temporal origin (7.8%) was significantly lower than that of non-temporal origin (17.2%) (P = 0.013). The percentage of oligoastrocytoma in gliomas of the temporal origin (7.0%) was significantly lower than that of non-temporal origin (22.0%) (P<0.001). The percentage of astrocytoma in gliomas of the insular origin (34.3%) was significantly higher than that of non-insular origin (18.3%) (P = 0.002). The percentage of oligoastrocytoma in gliomas of insular origin (32.9%) was significantly higher than that of non-insular origin (16.6%) (P = 0.001). The percentage of anaplastic astrocytoma in gliomas of the insular origin (1.4%) was significantly lower than that of non-insular origin (9.6%) (P = 0.022). The percentage of glioblastoma (5.7%) was significantly lower than that of non-insular origin (18.3%) (P = 0.008). A = astrocytoma; AA = anaplastic astrocytoma; G = glioblastoma; O = oligodendroglioma; AO = anaplastic oligodendroglioma; OA = oligoastrocytoma; AOA = anaplastic oligoastrocytoma.
Figure 2.
Gliomas of frontal and temporal origin had significantly different incidences of 1p/19q co-deletion irrespective and in respective of tumor pathology.
The regional incidences of 1p/19q co-deletion in all gliomas of the region irrespective of pathology were labeled with “All”. The regional incidences of 1p/19q co-deletion in respective of pathology were labeled with “A+AA+G, O+AO and OA+AOA” respectively. *The incidence of 1p/19q co-deletion in this region is significantly higher or lower than that in other regions (p<0.05, chi-square test).
Figure 3.
Gliomas of frontal and temporal origin had significantly different incidences of IDH1/2 mutation irrespective and in respective of tumor pathology.
The regional incidences of IDH1/2 mutation in all gliomas of the region irrespective of pathology were labeled with “All”. The regional incidences of IDH1/2 mutation in respective of pathology were labeled with “A+AA, O+AO and OA+AOA” respectively. *The incidence of IDH1/2 mutation in this region is significantly higher or lower than that in other regions (p<0.05, chi-square test).
Table 1.
Regional frequencies of 1p/19q co-deletion and IDH1/2 mutation in glioma subsets.
Table 2.
Regional molecular heterogeneity about chromosome 1p/19q and IDH1/2 in gliomas reported in English literature.