There are so many different types of cancer drugs coming into the clinic that it can sometimes be hard to keep up. Among the most exciting additions in the last decade are monoclonal antibodies (mAbs) – Herceptin and rituximab are two examples.
Rituximab was the first mAb to be licensed in the UK. It has transformed the outlook for many people with non-Hodgkin’s lymphoma and has just been approved for chronic lymphocytic leukaemia. But we still don’t fully understand how this and other mAbs work.
Cancer Research UK’s Professor Martin Glennie from the University of Southampton is an expert on antibody therapies. He gave a fascinating talk at the NCRI Cancer Conference on his latest research. In this short video, Professor Glennie and Dr Juliet Gray talk about their work on a new antibody treatment for neuroblastoma – a form of childhood cancer.
Hitting the target
In his presentation, Professor Glennie explained how mAbs work to fight cancer – by seeking out and attaching to specific proteins on the surface of cells, called antigens. They can then trigger the body’s immune system to destroy the tumour, or block important signals that the cancer cells need to grow and survive. Scientists are also looking to use mAbs to deliver a highly targeted dose of a drug or radiation to a cancer – a technique known as radio-immunotherapy.
As Professor Glennie went on to explain, the key to the success of any mAb drug is picking the right target. Rituximab and a number of other new drugs in the pipeline lock onto a particular antigen called CD20. Many scientists believe this to be the ‘perfect target’ – it’s the right shape and there is a lot of it (around 200,000 molecules on the surface of a single B-cell – the type of cell affected in non-Hodgkin’s lymphoma).
But Professor Glennie’s latest research suggests that when rituximab attaches to CD20 molecules on the surface of cancer cells, it causes the cells to ‘suck them up’ into their interior, along with the drug. This could make the drug less effective by reducing the availability of its target. And it appears that other so-called ‘type I’ antibodies – similar to rituximab – can also cause this effect.
Scientists are now on the case trying to understand exactly how and why this happens, and this knowledge could improve the potency of drugs like rituximab.
Also, scientists are studying ‘type II’ antibodies, which don’t seem to have the same effect on CD20. These alternative mAbs could become the next generation of treatments for tackling cancers like non-Hodgkin’s lymphoma and chronic lymphocytic leukaemia
Helen George, Head of Science Information
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