Scientists from the Manchester Collaborative Centre for Inflammation Research (MCCIR) have discovered why a particular cancer drug is so effective at killing cells. Their findings could be used to aid the design of future cancer treatments.
Professor Daniel Davis and his team used high quality video imaging to investigate why the drug rituximab is so effective at killing cancerous B cells. It is widely used in the treatment of B cell malignancies, such as lymphoma and leukaemia – as well as in autoimmune diseases like rheumatoid arthritis.
Using high-powered laser-based microscopes, researchers made videos of the process by which rituximab binds to a diseased cell and then attracts white blood cells known as natural killer (NK) cells to attack. They discovered that rituximab tended to stick to one side of the cancer cell, forming a cap and drawing a number of proteins over to that side. It effectively created a front and back to the cell – with a cluster of protein molecules massed on one side.
But what surprised the scientists most was how this changed the effectiveness of natural killer cells in destroying these diseased cells. When the NK cell latched onto the rituximab cap on the B cell, it had an 80% success rate at killing the cell. In contrast, when the B cell lacked this cluster of proteins on one side, it was killed only 40% of the time.
Tags: oncologia