Temozolomide and targeted therapy against epidermal growth factor receptor in glioma

Gliomas represent a heterogeneous group of diseases difficult to diagnose and even more difficult to treat. Intrinsic or acquired resistance to Temozolomide (TMZ) treatment is a common feature of both low- and high-grade glioma and is the major reason for therapeutic failure. The aim of this study is to improve the response to TMZ by blocking the Epithelial Growth Factor Receptor (EGFR) activity in glioma cells. GB1B and AC1B glioma cell lines used in this study were low passage cultures established from fresh tissues obtained from consented glioma patients undergoing surgery. Cell viability was quantified by hemocytometer cell counting, using trypan blue. Interactions between TMZ and EGFR inhibitor were classified by the Multiplicative Model. We found that TMZ treatment and inhibition of EGFR activity by AG556 suppressed tumor growth in glioblastoma and astrocytoma cells, but their co-administration induced additive and synergistic cell death in astrocytoma, whereas the treatment failed to elicit synergistic cytotoxicity in glioblastoma cells.