British researchers have unveiled a promising new approach to improving glioblastoma care.
Professor Susan Short of Leeds University, UK, and her team examined how glioblastoma can persist despite surgery and high-dose radiotherapy.
Resistance to radiotherapy is thought to be due to DNA double-strand break repair in stem-like cells, they say.
The team tested samples from glioblastoma patients and found that a repair protein called RAD51 is highly expressed in glioblastoma cells compared with normal brain cells.
Inhibitors of RAD51 called RI-1 and B02 can hold back this protein and limit DNA repair, the researchers report. This approach, together with radiation, could be an effective treatment for glioblastoma, they believe.
Findings were published last night (10 January) in Stem Cell Reports.
"Radiotherapy damages the DNA in the glioblastoma cells, but the RAD51 helps them to repair this damaged DNA, meaning they can repopulate the tumour," says Professor Short.
"By targeting RAD51 with an inhibitor we were able to make these glioblastoma cells more sensitive to the effects of radiotherapy, helping remove the tumour.
"The exact mechanism by which RAD51 becomes increased in cells that survive radiotherapy is not yet known but our study provides strong evidence that this is the right protein to target in the treatment of this aggressive brain cancer," she concludes.
Dr Justine Alford of Cancer Research UK commented: "This promising study in cells and mice may have found a way to cut off the tumour’s fuel supply, which could one day help treatments target the disease more precisely and effectively. But more research is needed to find out if this strategy could be safe and effective in people."
King, H. O. et al. RAD51 is a Selective DNA Repair Target to Radiosensitise Glioma Stem Cells. Stem Cell Reports.10 January 2017 doi: 10.1016/j.stemcr.2016.12.005 [abstract]
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