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Background: Malignant glioma are devastating tumors with poor prognosis. In recent years, the classification of glioma have evolved greatly due to exploration of several molecular tools in addition to the traditional immunohistochemistry.

Methods: To further evolve this classification, we thoroughly characterized the molecular and histological signature of 367 glioma patients from Sweden. We first obtained the full medical history and histological classification, along with matched blood samples and unstained tissue slides. We have performed extensive molecular characterization using genome wide association studies, methylation arrays and telomere length assays. We have extended the classification to include IDH1 mutations, chromosome 1p/19q co-deletion, EGFR amplification as well as the expression of two novel cell signaling regulators. The statistical analysis is ongoing and will reveal how well we can classify the tumors by combining the above mentioned techniques. 

Results: As expected we found EGFR upregulation in almost 50% of the patients with glioblastoma and one third of patients with anaplastic astrocytoma and anaplastic oligodendroglioma. No EGFR expression was found in any patient with low grade glioma. In consistence with previous studies 70% of the IDH1 mutated oligodendroglioma had 1p/19q co-deletion. In the IDH1 wildtype oligodendroglioma, about 50% of the low grade tumors had 1p/19q co-deletion. Interestingly, we found complete 1p/19q co-deletion in about 10% of the IDH1 wild type glioblastoma.

Conclusion: Today, 1p/19q co-deletion is normally only studied in suspected oligodendroglioma and not in all types of glioma. Pending the clinical relevance of the 1p/19q co-deleted glioblastoma, it might be wise to expand the 1p/19q classification by including all types of glioma.