As epidermal growth factor receptor (EGFR) has been reported to be a radiation 
response modulator, HER inhibitors are regarded to act as potential 
radiosensitisers. Our study examined the role of nimotuzumab and cetuximab both, 
the two monoclonal antibodies (mAbs) to EGFR, as radiosensitisers in a murine 
glioma model in vivo. Co-administration of both the antibodies with radiation 
increased the radiosensitivity of U87MG, resulting in a significant delay of 
subcutaneous (s.c.) tumour growth. Furthermore, the addition of antibodies to 
the radiation decreased brain tumour sizes and is inhibited by 40-80% the 
increased tumour cell invasion provoked by radiotherapy, although promoted 
tumour cell apoptosis. Whereas nimotuzumab led to a reduction in the size of 
tumour blood vessels and proliferating cells in s.c. tumours, cetuximab had no 
significant antiangiogenic nor antiproliferative activity. In contrast, 
cetuximab induced a more marked inhibition of EGFR downstream signalling 
compared with nimotuzumab. Moreover, both antibodies reduced the total number of 
radioresistant CD133+ cancer stem cells (CSCs). These results were encouraging, 
and showed the superiority of combined treatment of mAbs to EGFR and radiation 
over each single therapy against glioblastoma multiforme (GBM), confirming the 
role of these drugs as radiosensitisers in human GBM. In addition, we first 
showed the ability of mAb specifics against EGFR to target radioresistant glioma 
CSC, supporting the potential use in patients.