Radiosensitisers
Drugs given with radiotherapy to make tumour cells easier to kill: cisplatin in cervical and head and neck cancer, temozolomide in glioblastoma, nimorazole for hypoxic tumours, and a new generation aimed at DNA repair.
Overview
Concurrent chemoradiation is the commonest form of radiosensitisation: cisplatin with radiotherapy improved survival in cervical cancer in 1999 and in head and neck cancer soon after, temozolomide with radiotherapy did the same in glioblastoma, and 5-FU or capecitabine sensitises rectal and anal cancers. Cetuximab was the first targeted radiosensitiser. Hypoxic cell sensitisers such as nimorazole, standard in Danish head and neck practice, mimic oxygen in hypoxic cells. The next wave targets DNA damage repair (ATR, DNA-PK and PARP inhibitors), and hafnium oxide nanoparticles (NBTXR3) and gadolinium agents amplify the physical dose.
How it works
A drug lowers the dose of radiation needed to kill tumour cells, by blocking DNA repair, fixing damage in hypoxic cells, synchronising the cell cycle or increasing local energy deposition, ideally more in tumour than in normal tissue.
- Improved cure rates in several cancers
- Uses existing drugs
- Targets tumour-specific repair defects
- More acute toxicity
- Little sensitisation gain in some combinations
- Normal tissue may be sensitised too
NBTXR3 is Nanobiotix's radioenhancer: a single injection of hafnium oxide nanoparticles that makes ordinary radiotherapy hit harder inside the tumour. It carries a European CE mark for soft-tissue sarcoma and is in a phase 3 trial in head and neck cancer with Johnson and Johnson.
Nimorazole is the one hypoxic radiosensitiser in routine use: given with radiotherapy for head and neck cancer in Denmark since the DAHANCA 5 trial improved control, and tested across Europe in patients whose tumours carry a hypoxia gene signature.
Latest papers
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