How can we stop a fast growing leukaemia?
Cancer types:
Leukaemia
Project period:
–
Research institute:
University of Cambridge
Award amount:
£239,952
Location:
United Kingdom
Professor Brian Huntly hopes to discover a new way to treat acute myeloid leukaemia (AML) by exploring how a genetic mutation causes the cancer to grow. His team in Cambridge hope by better understanding how the leukaemia starts they can find clues towards a vital new cure.
Why is this research needed?
Acute myeloid leukaemia (AML) is an extremely aggressive blood cancer. It grows fast and can be difficult to treat. AML starts in white blood cells but we don’t yet fully understand what causes AML to develop.
What we do know is that there are some mutations in our genes that can make it more likely for AML to grow.
The team of Curestarter researchers now hope to discover how these mutations trigger AML development and also identify treatments that could stop them. This could lead to potential ways new cures for this cruel disease.
As a haematology consultant every week I see patients with blood cancers. Through research our options for treating many of them have improved significantly. However, there are still blood cancers that we find very hard to treat, and these include AML the disease that I specialise in most, where we urgently need new treatments. I find this slow progress motivates me to work harder to understand and find cures.
What is the science behind this project?
Your body is made up of millions of cells that all contain your DNA, the instruction book for how to run your body and keep you healthy. Sometimes mistakes – or mutations – can happen in these instructions. A lot of the time these mistakes are harmless but occasionally they mean that the instructions no longer make sense and the cell starts to misbehave. Tumours develop because cancer cells have mutations that cause them to divide uncontrollably.
In acute myeloid leukaemia (AML) there is a particular mutation called DNMT3A-R882 that appears to be involved in causing the disease and making it grow so quickly. Professor Huntly suspects that the mutation is doing this by altering how other genes are turned on through the way it interacts with other key molecules. Thanks to Curestarter support his team will use a combination of scientific techniques to map these interactions so that we can better understand the biological mechanisms behind how this mutation drives AML.
Excitingly it appears that some existing drugs could reverse the actions of the DNMT3A-R882 mutation – making the path from lab to clinic easier to navigate. As part of this cutting-edge project the team will test potential targets and therapies that could act on the DNMT3A-R882 mutation. By doing this they hope to discover much needed new ways to treat but also prevent or delay AML.
What difference could this project make to patients in the future?
Over 2,900 people in the UK are diagnosed with AML every year and unfortunately survival rates are particularly poor. Although current treatments will help some patients with AML, the cancer can grow very fast making it difficult to cure.
This innovative project will hopefully lead to a new treatment for AML that would mean patients have more time with their loved ones and fewer people have to say goodbye too soon.
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