Blocking a molecule may bypass bowel cancer's defense against the drug cetuximab, according to new research presented by Weir et al at the National Cancer Research Institute (NCRI) Cancer Conference in Liverpool, United Kingdom.
Cetuximab is used to treat advanced bowel cancer, and just under half of bowel cancer patients are given the drug. It works to block the epidermal growth factor receptor (EGFR). While it helps many patients, there are some for whom it doesn't work at all, and for others, it loses effectiveness.
Study Findings
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. But if they gave an ADAM 17 inhibitor known as IK682 to patients at the same time as cetuximab, the cancer cells died.
For other cancer cells, cetuximab treatment alone stopped them growing initially, but over time, they became resistant and started growing again. In these cases, the cancer cells were finding a way that didn't involve ADAM17, to outmaneuver the treatment.
Sandra Van Schaeybroeck, MD, lead researcher, 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.”
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