Blocking a molecule could bypass bowel cancer’s defence against the drug cetuximab, according to new research presented at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool.
Cetuximab is used to treat advanced bowel cancer, and just under half of bowel cancer patients are given the drug. While it helps many patients, there are some for whom it doesn’t work at all and for others it loses effectiveness.
To understand why this happens, scientists at Queen’s University Belfast treated bowel cancer cells in the lab with cetuximab. They found that some cells survived the treatment by increasing the activity of a protein called ADAM17.
Cetuximab works by blocking a molecule known as epidermal growth factor receptor (EGFR), which tells cells to grow.
There are around 41,000 cases of bowel cancer diagnosed in the UK each year. And each year around 16,000 die of the disease.
Dr Sandra Van Schaeybroeck, the lead researcher based at Queen’s University Belfast, said: “While some bowel cancer patients respond well to cetuximab treatment, many will relapse, or not benefit from the drug. Our work shows that combining this treatment with an ADAM17 inhibitor could be a promising avenue of therapy for patients who don’t respond to cetuximab by itself.
“More work is needed before we can safely test this combination in patients, but the prospect of cutting off cancer’s path to resistance is very exciting.”
“A big issue facing bowel cancer patients is the prospect of their cancer coming back. Understanding the mechanisms that bowel cancer cells use to evade treatment with cetuximab will help us find ways to delay or prevent it recurring. This will help more people with bowel cancer live longer and with better quality of life.”