Glioblastoma (GBM) is an aggressive form of brain cancer with a low survival rate, due in large part to resistance to temozolomide (TMZ), a DNA methylating agent used in combination with radiotherapy as first-line treatment after surgery. The major lesion induced by TMZ is methylated guanine (N7-meG), which is frequently lost from DNA creating toxic abasic sites (AP sites). AP sites are repaired through a Base Excision Repair (BER) pathway initiated either by AP endonucleases or by AP lyases. It is generally assumed that AP endonucleases play a major role, but the contribution of AP lyases to TMZ-resistance remains largely unknown. Furthermore, unprocessed AP sites may generate single- and double-strand DNA breaks, channelling repair through alternative, BER-independent routes. Since DNA repair mechanisms contribute to TMZ resistance and are epigenetically regulated, tumour-specific DNA repair and epigenetic signatures may be used as predictive biomarkers of patient response to treatment. In this context, in order to move towards personalised therapy in cancer treatment, GLIOCHEM aims to generate new knowledge about the causes of resistance to TMZ in GBM cell lines, allowing the identification of biomarkers than can predict response to treatment and the identification of new therapeutic targets.